rabbit monoclonal eno1  (Abcam)

 
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    Abcam rabbit monoclonal eno1
    Source, application and concentration of antibodies.
    Rabbit Monoclonal Eno1, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit monoclonal eno1/product/Abcam
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbit monoclonal eno1 - by Bioz Stars, 2023-10
    86/100 stars

    Images

    1) Product Images from "Helicase-like transcription factor (HLTF) -deleted CDX/TME model of colorectal cancer increased transcription of oxidative phosphorylation genes and diverted glycolysis to boost S-glutathionylation in lymphatic intravascular metastatic niches"

    Article Title: Helicase-like transcription factor (HLTF) -deleted CDX/TME model of colorectal cancer increased transcription of oxidative phosphorylation genes and diverted glycolysis to boost S-glutathionylation in lymphatic intravascular metastatic niches

    Journal: PLOS ONE

    doi: 10.1371/journal.pone.0291023

    Source, application and concentration of antibodies.
    Figure Legend Snippet: Source, application and concentration of antibodies.

    Techniques Used: Concentration Assay, Recombinant, Plasmid Preparation

    Summary of site-specific S-glutathionylation identified by 2D-DIGE MALDI-TOF/TOF mass spectrometry. Pr-SSG in HLTF -/- CDX/TME.
    Figure Legend Snippet: Summary of site-specific S-glutathionylation identified by 2D-DIGE MALDI-TOF/TOF mass spectrometry. Pr-SSG in HLTF -/- CDX/TME.

    Techniques Used: Mass Spectrometry

    anti eno1 2 3 ab189891 antibodies  (Abcam)

     
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    Abcam anti eno1 2 3 ab189891 antibodies
    Anti Eno1 2 3 Ab189891 Antibodies, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti eno1 2 3 ab189891 antibodies/product/Abcam
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti eno1 2 3 ab189891 antibodies - by Bioz Stars, 2023-10
    86/100 stars

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    eno1 antibodies  (Abcam)

     
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    Abcam eno1 antibodies
    The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between <t>ENO1,</t> GRN, and PTGS2 with immune infiltrating cells.
    Eno1 Antibodies, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/eno1 antibodies/product/Abcam
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    eno1 antibodies - by Bioz Stars, 2023-10
    86/100 stars

    Images

    1) Product Images from "Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis"

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2023.1197275

    The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between ENO1, GRN, and PTGS2 with immune infiltrating cells.
    Figure Legend Snippet: The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between ENO1, GRN, and PTGS2 with immune infiltrating cells.

    Techniques Used:

    GWAS analysis to identify the pathogenic regions of the hub genes. The Manhattan plot shows the SNP pathogenic regions corresponding to PTGS2, ENO1 and GRN.
    Figure Legend Snippet: GWAS analysis to identify the pathogenic regions of the hub genes. The Manhattan plot shows the SNP pathogenic regions corresponding to PTGS2, ENO1 and GRN.

    Techniques Used:

    GSEA analysis of hub genes. (A) The top 3 most enriched pathways about function enrichment of PTGS2 gene: Nod-like receptor signaling pathway, gene set enriched in FcγR mediated phagocytosis, gene set enriched in the Chemokine signaling pathway. (B) The top 3 most enriched pathways about function enrichment of GRN gene: Lysosome, Leishmania infection, B cell receptor signaling pathway. (C) The top 3 most enriched pathways about function enrichment of ENO1 gene: Lysosome, Pathogenic Escherichia coli infection, Leishmania infection. Screening criteria for significant gene sets included adj. p-value < 0.05 and FDR < 0.5. NES, normalized enrichment score.
    Figure Legend Snippet: GSEA analysis of hub genes. (A) The top 3 most enriched pathways about function enrichment of PTGS2 gene: Nod-like receptor signaling pathway, gene set enriched in FcγR mediated phagocytosis, gene set enriched in the Chemokine signaling pathway. (B) The top 3 most enriched pathways about function enrichment of GRN gene: Lysosome, Leishmania infection, B cell receptor signaling pathway. (C) The top 3 most enriched pathways about function enrichment of ENO1 gene: Lysosome, Pathogenic Escherichia coli infection, Leishmania infection. Screening criteria for significant gene sets included adj. p-value < 0.05 and FDR < 0.5. NES, normalized enrichment score.

    Techniques Used: Infection

    Enrichment analysis for transcription factors of hub genes (A) Histogram of the AUC. By calculating the AUC, the over-representation of each motif for hub genes was assessed. Red vertical line indicates the degree of significance, whereby motifs with AUC higher than the significance level are considered significant motifs. (B) The recovery curve for the three most significant motifs. Red line represents the global mean of recovered motif curve, green line represents the mean ± standard deviation. Motifs that were larger than the mean ± standard deviation were considered statistically significant. Blue line represents the current motif’s recovered curve. The motif cisbp_M5493 was significantly enriched in hub genes (ENO1 and PTGS2).
    Figure Legend Snippet: Enrichment analysis for transcription factors of hub genes (A) Histogram of the AUC. By calculating the AUC, the over-representation of each motif for hub genes was assessed. Red vertical line indicates the degree of significance, whereby motifs with AUC higher than the significance level are considered significant motifs. (B) The recovery curve for the three most significant motifs. Red line represents the global mean of recovered motif curve, green line represents the mean ± standard deviation. Motifs that were larger than the mean ± standard deviation were considered statistically significant. Blue line represents the current motif’s recovered curve. The motif cisbp_M5493 was significantly enriched in hub genes (ENO1 and PTGS2).

    Techniques Used: Standard Deviation

    Single-cell analysis revealed the expression of PTGS2, ENO1 and GRN. (A) Dot plot of hub genes for each cell type. (B) Violin plots showing the expression level of hub genes in nine cell type.
    Figure Legend Snippet: Single-cell analysis revealed the expression of PTGS2, ENO1 and GRN. (A) Dot plot of hub genes for each cell type. (B) Violin plots showing the expression level of hub genes in nine cell type.

    Techniques Used: Single-cell Analysis, Expressing

    Validation of the hub genes in experimental samples. (A) Representative tracing of the PI and the joint swelling thickness in rat after CFA or Nor treatment in the two groups(n=12). (B) Representative images of H&E staining of joint sections from AIA rat or Nor rat. (C) The expression of GRN, PTGS2 and ENO1. n = 3. *p < 0.05, **p < 0.01, ***p < 0.001. (D) IHC staining for PTGS2, ENO1, and GRN on synovium from samples of OA and RA patients (n = 3).
    Figure Legend Snippet: Validation of the hub genes in experimental samples. (A) Representative tracing of the PI and the joint swelling thickness in rat after CFA or Nor treatment in the two groups(n=12). (B) Representative images of H&E staining of joint sections from AIA rat or Nor rat. (C) The expression of GRN, PTGS2 and ENO1. n = 3. *p < 0.05, **p < 0.01, ***p < 0.001. (D) IHC staining for PTGS2, ENO1, and GRN on synovium from samples of OA and RA patients (n = 3).

    Techniques Used: Staining, Expressing, Immunohistochemistry

    (A) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model with knockdown of ENO1-siRNA (n=3). (B) The expression level of ENO1 and ACO1 in primary FLS of RA patients(n=3). (C, D) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model and RA patients with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/) (n=3). (E) The assessment of cell viability by CCK-8 assay in primary FLS of rat models with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ### P < 0.001 versus siRNA group. ****P < 0.0001 versus siRNA group; #P < 0.05 and ## P < 0.01 versus siRNA+Fe2+group. (F) The assessment of cell viability by CCK-8 assay in primary FLS of RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ###P < 0.001 versus siRNA group. *P < 0.05 versus siRNA group; # P < 0.05 versus siRNA+Fe 2+ group.
    Figure Legend Snippet: (A) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model with knockdown of ENO1-siRNA (n=3). (B) The expression level of ENO1 and ACO1 in primary FLS of RA patients(n=3). (C, D) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model and RA patients with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/) (n=3). (E) The assessment of cell viability by CCK-8 assay in primary FLS of rat models with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ### P < 0.001 versus siRNA group. ****P < 0.0001 versus siRNA group; #P < 0.05 and ## P < 0.01 versus siRNA+Fe2+group. (F) The assessment of cell viability by CCK-8 assay in primary FLS of RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ###P < 0.001 versus siRNA group. *P < 0.05 versus siRNA group; # P < 0.05 versus siRNA+Fe 2+ group.

    Techniques Used: Expressing, CCK-8 Assay

    The assessment of lipid peroxidation by flow cytometry in primary FLS of rat model (A) and RA patients (B) with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). (C) The assessment of Intracellular ferrous ion by cellular ferrous ion detection fluorescent probes in primary FLS of rat model and RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/).
    Figure Legend Snippet: The assessment of lipid peroxidation by flow cytometry in primary FLS of rat model (A) and RA patients (B) with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). (C) The assessment of Intracellular ferrous ion by cellular ferrous ion detection fluorescent probes in primary FLS of rat model and RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/).

    Techniques Used: Flow Cytometry

    eno1  (Abcam)

     
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    Abcam eno1
    The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between <t>ENO1,</t> GRN, and PTGS2 with immune infiltrating cells.
    Eno1, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/eno1/product/Abcam
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    eno1 - by Bioz Stars, 2023-10
    86/100 stars

    Images

    1) Product Images from "Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis"

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    Journal: Frontiers in Immunology

    doi: 10.3389/fimmu.2023.1197275

    The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between ENO1, GRN, and PTGS2 with immune infiltrating cells.
    Figure Legend Snippet: The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between ENO1, GRN, and PTGS2 with immune infiltrating cells.

    Techniques Used:

    GWAS analysis to identify the pathogenic regions of the hub genes. The Manhattan plot shows the SNP pathogenic regions corresponding to PTGS2, ENO1 and GRN.
    Figure Legend Snippet: GWAS analysis to identify the pathogenic regions of the hub genes. The Manhattan plot shows the SNP pathogenic regions corresponding to PTGS2, ENO1 and GRN.

    Techniques Used:

    GSEA analysis of hub genes. (A) The top 3 most enriched pathways about function enrichment of PTGS2 gene: Nod-like receptor signaling pathway, gene set enriched in FcγR mediated phagocytosis, gene set enriched in the Chemokine signaling pathway. (B) The top 3 most enriched pathways about function enrichment of GRN gene: Lysosome, Leishmania infection, B cell receptor signaling pathway. (C) The top 3 most enriched pathways about function enrichment of ENO1 gene: Lysosome, Pathogenic Escherichia coli infection, Leishmania infection. Screening criteria for significant gene sets included adj. p-value < 0.05 and FDR < 0.5. NES, normalized enrichment score.
    Figure Legend Snippet: GSEA analysis of hub genes. (A) The top 3 most enriched pathways about function enrichment of PTGS2 gene: Nod-like receptor signaling pathway, gene set enriched in FcγR mediated phagocytosis, gene set enriched in the Chemokine signaling pathway. (B) The top 3 most enriched pathways about function enrichment of GRN gene: Lysosome, Leishmania infection, B cell receptor signaling pathway. (C) The top 3 most enriched pathways about function enrichment of ENO1 gene: Lysosome, Pathogenic Escherichia coli infection, Leishmania infection. Screening criteria for significant gene sets included adj. p-value < 0.05 and FDR < 0.5. NES, normalized enrichment score.

    Techniques Used: Infection

    Enrichment analysis for transcription factors of hub genes (A) Histogram of the AUC. By calculating the AUC, the over-representation of each motif for hub genes was assessed. Red vertical line indicates the degree of significance, whereby motifs with AUC higher than the significance level are considered significant motifs. (B) The recovery curve for the three most significant motifs. Red line represents the global mean of recovered motif curve, green line represents the mean ± standard deviation. Motifs that were larger than the mean ± standard deviation were considered statistically significant. Blue line represents the current motif’s recovered curve. The motif cisbp_M5493 was significantly enriched in hub genes (ENO1 and PTGS2).
    Figure Legend Snippet: Enrichment analysis for transcription factors of hub genes (A) Histogram of the AUC. By calculating the AUC, the over-representation of each motif for hub genes was assessed. Red vertical line indicates the degree of significance, whereby motifs with AUC higher than the significance level are considered significant motifs. (B) The recovery curve for the three most significant motifs. Red line represents the global mean of recovered motif curve, green line represents the mean ± standard deviation. Motifs that were larger than the mean ± standard deviation were considered statistically significant. Blue line represents the current motif’s recovered curve. The motif cisbp_M5493 was significantly enriched in hub genes (ENO1 and PTGS2).

    Techniques Used: Standard Deviation

    Single-cell analysis revealed the expression of PTGS2, ENO1 and GRN. (A) Dot plot of hub genes for each cell type. (B) Violin plots showing the expression level of hub genes in nine cell type.
    Figure Legend Snippet: Single-cell analysis revealed the expression of PTGS2, ENO1 and GRN. (A) Dot plot of hub genes for each cell type. (B) Violin plots showing the expression level of hub genes in nine cell type.

    Techniques Used: Single-cell Analysis, Expressing

    Validation of the hub genes in experimental samples. (A) Representative tracing of the PI and the joint swelling thickness in rat after CFA or Nor treatment in the two groups(n=12). (B) Representative images of H&E staining of joint sections from AIA rat or Nor rat. (C) The expression of GRN, PTGS2 and ENO1. n = 3. *p < 0.05, **p < 0.01, ***p < 0.001. (D) IHC staining for PTGS2, ENO1, and GRN on synovium from samples of OA and RA patients (n = 3).
    Figure Legend Snippet: Validation of the hub genes in experimental samples. (A) Representative tracing of the PI and the joint swelling thickness in rat after CFA or Nor treatment in the two groups(n=12). (B) Representative images of H&E staining of joint sections from AIA rat or Nor rat. (C) The expression of GRN, PTGS2 and ENO1. n = 3. *p < 0.05, **p < 0.01, ***p < 0.001. (D) IHC staining for PTGS2, ENO1, and GRN on synovium from samples of OA and RA patients (n = 3).

    Techniques Used: Staining, Expressing, Immunohistochemistry

    (A) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model with knockdown of ENO1-siRNA (n=3). (B) The expression level of ENO1 and ACO1 in primary FLS of RA patients(n=3). (C, D) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model and RA patients with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/) (n=3). (E) The assessment of cell viability by CCK-8 assay in primary FLS of rat models with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ### P < 0.001 versus siRNA group. ****P < 0.0001 versus siRNA group; #P < 0.05 and ## P < 0.01 versus siRNA+Fe2+group. (F) The assessment of cell viability by CCK-8 assay in primary FLS of RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ###P < 0.001 versus siRNA group. *P < 0.05 versus siRNA group; # P < 0.05 versus siRNA+Fe 2+ group.
    Figure Legend Snippet: (A) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model with knockdown of ENO1-siRNA (n=3). (B) The expression level of ENO1 and ACO1 in primary FLS of RA patients(n=3). (C, D) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model and RA patients with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/) (n=3). (E) The assessment of cell viability by CCK-8 assay in primary FLS of rat models with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ### P < 0.001 versus siRNA group. ****P < 0.0001 versus siRNA group; #P < 0.05 and ## P < 0.01 versus siRNA+Fe2+group. (F) The assessment of cell viability by CCK-8 assay in primary FLS of RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ###P < 0.001 versus siRNA group. *P < 0.05 versus siRNA group; # P < 0.05 versus siRNA+Fe 2+ group.

    Techniques Used: Expressing, CCK-8 Assay

    The assessment of lipid peroxidation by flow cytometry in primary FLS of rat model (A) and RA patients (B) with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). (C) The assessment of Intracellular ferrous ion by cellular ferrous ion detection fluorescent probes in primary FLS of rat model and RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/).
    Figure Legend Snippet: The assessment of lipid peroxidation by flow cytometry in primary FLS of rat model (A) and RA patients (B) with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). (C) The assessment of Intracellular ferrous ion by cellular ferrous ion detection fluorescent probes in primary FLS of rat model and RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/).

    Techniques Used: Flow Cytometry

    rabbitanti eno1 antibodies  (Abcam)

     
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    Abcam rabbitanti eno1 antibodies
    Rabbitanti Eno1 Antibodies, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbitanti eno1 antibodies/product/Abcam
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    rabbitanti eno1 antibodies - by Bioz Stars, 2023-10
    86/100 stars

    Images

    eno1  (Abcam)

     
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    Abcam eno1
    <t>ENO1</t> expression in villous tissues and trophoblast cells. (a–c) ENO1 mRNA and protein levels in villous tissue of patients with RM compared with that of women for induced abortion were detected by qRT‐PCR and western blot analyses; (d–f) ENO1 mRNA and protein levels in trophoblast‐derived cell lines were tested by qRT‐PCR and western blot analyses. ** p < 0.01; *** p < 0.001. RM, recurrent miscarriage.
    Eno1, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/eno1/product/Abcam
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    eno1 - by Bioz Stars, 2023-10
    86/100 stars

    Images

    1) Product Images from "Alpha‐enolase 1 knockdown facilitates the proliferation and invasion of villous trophoblasts by upregulating COX ‐2"

    Article Title: Alpha‐enolase 1 knockdown facilitates the proliferation and invasion of villous trophoblasts by upregulating COX ‐2

    Journal: Molecular Genetics & Genomic Medicine

    doi: 10.1002/mgg3.2220

    ENO1 expression in villous tissues and trophoblast cells. (a–c) ENO1 mRNA and protein levels in villous tissue of patients with RM compared with that of women for induced abortion were detected by qRT‐PCR and western blot analyses; (d–f) ENO1 mRNA and protein levels in trophoblast‐derived cell lines were tested by qRT‐PCR and western blot analyses. ** p < 0.01; *** p < 0.001. RM, recurrent miscarriage.
    Figure Legend Snippet: ENO1 expression in villous tissues and trophoblast cells. (a–c) ENO1 mRNA and protein levels in villous tissue of patients with RM compared with that of women for induced abortion were detected by qRT‐PCR and western blot analyses; (d–f) ENO1 mRNA and protein levels in trophoblast‐derived cell lines were tested by qRT‐PCR and western blot analyses. ** p < 0.01; *** p < 0.001. RM, recurrent miscarriage.

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot, Derivative Assay

    ENO1 localization and expression in villous tissues of RM patients. (a and b) Immunohistochemistry analysis of ENO1 stain from placental villus of RM patients and women for induced abortion. The cell membranes of villous trophoblast cells in patients with RM were dark brown, while those in the control group appeared light yellow. RM, recurrent miscarriage.
    Figure Legend Snippet: ENO1 localization and expression in villous tissues of RM patients. (a and b) Immunohistochemistry analysis of ENO1 stain from placental villus of RM patients and women for induced abortion. The cell membranes of villous trophoblast cells in patients with RM were dark brown, while those in the control group appeared light yellow. RM, recurrent miscarriage.

    Techniques Used: Expressing, Immunohistochemistry, Staining

    Effects of ENO1 on trophoblast proliferation, migration and invasion. (a–c) qRT‐PCR and western blot analyses of ENO1 level in ENO1‐downregulated Bewo cells. (d) CCK8 assay of Bewo cell proliferation after ENO1 depletion. (e and f) Transwell chamber assays were employed to evaluate Bewo cell migratory and invasive capabilities affected by ENO1 knockdown. (g and h) Western blot analysis of the expression of EMT markers in ENO1‐downregulated Bewo cells. * p < 0.05; ** p < 0.01; *** p < 0.001.
    Figure Legend Snippet: Effects of ENO1 on trophoblast proliferation, migration and invasion. (a–c) qRT‐PCR and western blot analyses of ENO1 level in ENO1‐downregulated Bewo cells. (d) CCK8 assay of Bewo cell proliferation after ENO1 depletion. (e and f) Transwell chamber assays were employed to evaluate Bewo cell migratory and invasive capabilities affected by ENO1 knockdown. (g and h) Western blot analysis of the expression of EMT markers in ENO1‐downregulated Bewo cells. * p < 0.05; ** p < 0.01; *** p < 0.001.

    Techniques Used: Migration, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Expressing

    Effects of ENO1 knockdown on the expression of COX‐2, c‐Myc and cyclin D1. (a–c) RT‐qPCR and western blot analyses of the expression of COX‐2, c‐Myc and cyclin D1 in Bewo cells after downregulating ENO1. **p < 0.01; *** p < 0.001.
    Figure Legend Snippet: Effects of ENO1 knockdown on the expression of COX‐2, c‐Myc and cyclin D1. (a–c) RT‐qPCR and western blot analyses of the expression of COX‐2, c‐Myc and cyclin D1 in Bewo cells after downregulating ENO1. **p < 0.01; *** p < 0.001.

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot

    The schematic diagram illustrating the molecular mechanism involved in the regulation of ENO1 for RM development.
    Figure Legend Snippet: The schematic diagram illustrating the molecular mechanism involved in the regulation of ENO1 for RM development.

    Techniques Used:

    eno1  (Abcam)

     
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    Abcam eno1
    Eno1, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    eno1 - by Bioz Stars, 2023-10
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    eno1 antibody  (Abcam)

     
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    Abcam eno1 antibody
    Characterization of the <t>ENO1</t> -RNA interaction profile by an iRIP-seq analysis. (A) Experimental and computational work flow of the iRIP-seq. (B) Western blot analysis of the ENO1 immunoprecipitates using anti-Flag monoclonal antibody. Two replicates were performed. (C) Sample cluster analysis plots. (D) Sample correlation analysis. (E) A pie chart showing the genomic distribution of the ENO1 -bound peaks from the two biological replicates. (F) The motif analysis results showing the enriched motifs from the ENO1 -bound peaks from the two biological replicates. (G) The distribution of the GACGAGGA enrichment sequences in both experiments in the Ablife analysis. (H) A Venn diagram showing the overlapping peaks between IP-1 and IP-2. (I) A scatter plot showing the most enriched GO biological process (left panel) and KEGG pathway (right panel) results of the overlapping peak genes. ENO1 , enolase 1; IgG, immunoglobulin G; RT-PCR, reverse transcription-polymerase chain reaction; IP, immunoprecipitation; PPIA, peptidylprolyl isomerase A; 3'UTR, 3' untranslated region; 5'UTR, 5' untranslated region; CDS, coding sequence; nc, non-coding; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; iRIP-seq, improved RNA immunoprecipitation and deep sequencing.
    Eno1 Antibody, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    eno1 antibody - by Bioz Stars, 2023-10
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    1) Product Images from "RNA-binding protein ENO1 promotes the tumor progression of gastric cancer by binding to and regulating gastric cancer-related genes"

    Article Title: RNA-binding protein ENO1 promotes the tumor progression of gastric cancer by binding to and regulating gastric cancer-related genes

    Journal: Journal of Gastrointestinal Oncology

    doi: 10.21037/jgo-23-151

    Characterization of the ENO1 -RNA interaction profile by an iRIP-seq analysis. (A) Experimental and computational work flow of the iRIP-seq. (B) Western blot analysis of the ENO1 immunoprecipitates using anti-Flag monoclonal antibody. Two replicates were performed. (C) Sample cluster analysis plots. (D) Sample correlation analysis. (E) A pie chart showing the genomic distribution of the ENO1 -bound peaks from the two biological replicates. (F) The motif analysis results showing the enriched motifs from the ENO1 -bound peaks from the two biological replicates. (G) The distribution of the GACGAGGA enrichment sequences in both experiments in the Ablife analysis. (H) A Venn diagram showing the overlapping peaks between IP-1 and IP-2. (I) A scatter plot showing the most enriched GO biological process (left panel) and KEGG pathway (right panel) results of the overlapping peak genes. ENO1 , enolase 1; IgG, immunoglobulin G; RT-PCR, reverse transcription-polymerase chain reaction; IP, immunoprecipitation; PPIA, peptidylprolyl isomerase A; 3'UTR, 3' untranslated region; 5'UTR, 5' untranslated region; CDS, coding sequence; nc, non-coding; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; iRIP-seq, improved RNA immunoprecipitation and deep sequencing.
    Figure Legend Snippet: Characterization of the ENO1 -RNA interaction profile by an iRIP-seq analysis. (A) Experimental and computational work flow of the iRIP-seq. (B) Western blot analysis of the ENO1 immunoprecipitates using anti-Flag monoclonal antibody. Two replicates were performed. (C) Sample cluster analysis plots. (D) Sample correlation analysis. (E) A pie chart showing the genomic distribution of the ENO1 -bound peaks from the two biological replicates. (F) The motif analysis results showing the enriched motifs from the ENO1 -bound peaks from the two biological replicates. (G) The distribution of the GACGAGGA enrichment sequences in both experiments in the Ablife analysis. (H) A Venn diagram showing the overlapping peaks between IP-1 and IP-2. (I) A scatter plot showing the most enriched GO biological process (left panel) and KEGG pathway (right panel) results of the overlapping peak genes. ENO1 , enolase 1; IgG, immunoglobulin G; RT-PCR, reverse transcription-polymerase chain reaction; IP, immunoprecipitation; PPIA, peptidylprolyl isomerase A; 3'UTR, 3' untranslated region; 5'UTR, 5' untranslated region; CDS, coding sequence; nc, non-coding; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; iRIP-seq, improved RNA immunoprecipitation and deep sequencing.

    Techniques Used: Western Blot, Reverse Transcription Polymerase Chain Reaction, Immunoprecipitation, Sequencing

    ENO1 binds to genes related to the occurrence and development of GC. (A) The ENO1 -binding peak genes of NEAT1 . Left panel: an IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and red panels represent the positions of the peaks. The distribution reads of the bound gene are plotted in the upper panel and the transcripts of each gene are shown below. Right panel: a bar plot showing the FPKM of NEAT1 . (B) The ENO1 -binding peak genes of PKM . Left panel: an IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and blue panels represent the positions of the peaks. The distribution reads of the bound gene is plotted in the upper panel and the transcripts of each gene are shown below. Right panel: a bar plot showing the FPKM of PKM . (C) The ENO1 -binding peak genes of CD44 . Left panel: an IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and red panels represent the positions of the peaks. The distribution reads of the bound gene is plotted in the upper panel, and the transcripts of each gene are shown below. Right panel: a bar plot showing the FPKM of CD44 . **, P<0.05; ***, P<0.001. ENO1, enolase 1; IP, immunoprecipitation; NEAT1, nuclear enriched abundant transcript 1; PKM, pyruvate kinase M; GC, gastric cancer; IGV, Integrative Genomics Viewer; FPKM, fragments per kilobase million.
    Figure Legend Snippet: ENO1 binds to genes related to the occurrence and development of GC. (A) The ENO1 -binding peak genes of NEAT1 . Left panel: an IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and red panels represent the positions of the peaks. The distribution reads of the bound gene are plotted in the upper panel and the transcripts of each gene are shown below. Right panel: a bar plot showing the FPKM of NEAT1 . (B) The ENO1 -binding peak genes of PKM . Left panel: an IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and blue panels represent the positions of the peaks. The distribution reads of the bound gene is plotted in the upper panel and the transcripts of each gene are shown below. Right panel: a bar plot showing the FPKM of PKM . (C) The ENO1 -binding peak genes of CD44 . Left panel: an IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and red panels represent the positions of the peaks. The distribution reads of the bound gene is plotted in the upper panel, and the transcripts of each gene are shown below. Right panel: a bar plot showing the FPKM of CD44 . **, P<0.05; ***, P<0.001. ENO1, enolase 1; IP, immunoprecipitation; NEAT1, nuclear enriched abundant transcript 1; PKM, pyruvate kinase M; GC, gastric cancer; IGV, Integrative Genomics Viewer; FPKM, fragments per kilobase million.

    Techniques Used: Binding Assay, Immunoprecipitation

    The ENO1 -interaction regulates the expression of the target genes associated with GC. The differentially expressed genes were output by using the data of previous gene chip sequencing. (A) Left panel: a Venn diagram showing the overlapping genes between the ENO1 -bound peaks in the fRIP-seq and the upregulated DEGs. Right panel: the overlapping genes between the ENO1 -bound peaks in the fRIP-seq and the downregulated DEGs. (B) A bar plot showing the expression pattern and statistical differences of the upregulated DEGs in the overlapping genes. The error bars represent the mean ± SEM. (C) A bar plot showing the expression pattern and statistical difference of the downregulated DEGs in the overlapping genes. The error bars represent the mean ± SEM. (D) The ENO1 -binding peak genes of MCL1 . An IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and blue panels represent the positions of the peaks. The read distribution of the bound gene is plotted in the upper panel and the transcripts of each gene are shown below. (E) The ENO1 -binding peak genes of SOX9 . An IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and blue panels represent the positions of the peaks. The read distribution of the bound gene is plotted in the upper panel and the transcripts of each gene are shown above. ***, P<0.001. DEG, differentially expressed gene; IP, immunoprecipitation; NC, negative control; KD, knockdown; MCL1, myeloid cell leukemia 1; VEGFA, vascular endothelial growth factor A; SOX9, SRY-box transcription factor 9; ENO1, enolase 1; GC, gastric cancer; fRIP-seq, formaldehyde crosslinking RNA immunoprecipitation sequencing; SEM, standard error of the mean; IGV, Integrative Genomics Viewer.
    Figure Legend Snippet: The ENO1 -interaction regulates the expression of the target genes associated with GC. The differentially expressed genes were output by using the data of previous gene chip sequencing. (A) Left panel: a Venn diagram showing the overlapping genes between the ENO1 -bound peaks in the fRIP-seq and the upregulated DEGs. Right panel: the overlapping genes between the ENO1 -bound peaks in the fRIP-seq and the downregulated DEGs. (B) A bar plot showing the expression pattern and statistical differences of the upregulated DEGs in the overlapping genes. The error bars represent the mean ± SEM. (C) A bar plot showing the expression pattern and statistical difference of the downregulated DEGs in the overlapping genes. The error bars represent the mean ± SEM. (D) The ENO1 -binding peak genes of MCL1 . An IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and blue panels represent the positions of the peaks. The read distribution of the bound gene is plotted in the upper panel and the transcripts of each gene are shown below. (E) The ENO1 -binding peak genes of SOX9 . An IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and blue panels represent the positions of the peaks. The read distribution of the bound gene is plotted in the upper panel and the transcripts of each gene are shown above. ***, P<0.001. DEG, differentially expressed gene; IP, immunoprecipitation; NC, negative control; KD, knockdown; MCL1, myeloid cell leukemia 1; VEGFA, vascular endothelial growth factor A; SOX9, SRY-box transcription factor 9; ENO1, enolase 1; GC, gastric cancer; fRIP-seq, formaldehyde crosslinking RNA immunoprecipitation sequencing; SEM, standard error of the mean; IGV, Integrative Genomics Viewer.

    Techniques Used: Expressing, ChIP-sequencing, Binding Assay, Immunoprecipitation, Negative Control, Sequencing

    eno1  (Abcam)

     
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    Abcam eno1
    <t>Eno1</t> was upregulated in icariin-induced osteogenic differentiation. (A) Venn analysis of targets of postmenopausal osteoporosis (PMOP) and diabetes mellitus (DM). (B) KEGG pathway enrichment analysis was performed. Red box indicates HIF-1 signalling pathway. (C) Protein-protein interaction network was built and Eno1 was marked in red. (D)mRNA levels of Eno1 was tested by qPCR. All the data are shown as mean ± SD (n = 3) in three independent experiments. (E) Western Blot analysis for Eno1 was performed. Vinculin was used as a reference protein. Relative expression of Eno1(F) were normalized against Vinculin. * P ＜0.05, *** P ＜0.001 versus the blank control group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
    Eno1, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    eno1 - by Bioz Stars, 2023-10
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    1) Product Images from "Icariin promotes osteogenic differentiation by upregulating alpha-enolase expression"

    Article Title: Icariin promotes osteogenic differentiation by upregulating alpha-enolase expression

    Journal: Biochemistry and Biophysics Reports

    doi: 10.1016/j.bbrep.2023.101471

    Eno1 was upregulated in icariin-induced osteogenic differentiation. (A) Venn analysis of targets of postmenopausal osteoporosis (PMOP) and diabetes mellitus (DM). (B) KEGG pathway enrichment analysis was performed. Red box indicates HIF-1 signalling pathway. (C) Protein-protein interaction network was built and Eno1 was marked in red. (D)mRNA levels of Eno1 was tested by qPCR. All the data are shown as mean ± SD (n = 3) in three independent experiments. (E) Western Blot analysis for Eno1 was performed. Vinculin was used as a reference protein. Relative expression of Eno1(F) were normalized against Vinculin. * P ＜0.05, *** P ＜0.001 versus the blank control group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
    Figure Legend Snippet: Eno1 was upregulated in icariin-induced osteogenic differentiation. (A) Venn analysis of targets of postmenopausal osteoporosis (PMOP) and diabetes mellitus (DM). (B) KEGG pathway enrichment analysis was performed. Red box indicates HIF-1 signalling pathway. (C) Protein-protein interaction network was built and Eno1 was marked in red. (D)mRNA levels of Eno1 was tested by qPCR. All the data are shown as mean ± SD (n = 3) in three independent experiments. (E) Western Blot analysis for Eno1 was performed. Vinculin was used as a reference protein. Relative expression of Eno1(F) were normalized against Vinculin. * P ＜0.05, *** P ＜0.001 versus the blank control group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

    Techniques Used: Western Blot, Expressing

    Inhibition of Eno1 weakened icariin-induced osteogenic differentiation. (A) Cell viability of MC3T3-E1 under different concentration of ENOblock were measured by CCK8 assay for 24, 48, 72h. (B) The mineralization of 21-days induction with or without ENOblock and icariin were performed by Alizarin red S staining, and calcium deposits were quantified by measuring OD 562 after destaining (C). (D–F) mRNA levels of Alp (D), Bgp (E) and Runx2 (F), were tested as osteogenic markers by qPCR. All the data are shown as mean ± SD (n = 3) in three independent experiments. * P ＜0.05, ** P ＜0.01, **** P ＜0.0001 versus the blank control group, && P ＜0.01, &&&& P ＜0.0001 versus the icariin group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
    Figure Legend Snippet: Inhibition of Eno1 weakened icariin-induced osteogenic differentiation. (A) Cell viability of MC3T3-E1 under different concentration of ENOblock were measured by CCK8 assay for 24, 48, 72h. (B) The mineralization of 21-days induction with or without ENOblock and icariin were performed by Alizarin red S staining, and calcium deposits were quantified by measuring OD 562 after destaining (C). (D–F) mRNA levels of Alp (D), Bgp (E) and Runx2 (F), were tested as osteogenic markers by qPCR. All the data are shown as mean ± SD (n = 3) in three independent experiments. * P ＜0.05, ** P ＜0.01, **** P ＜0.0001 versus the blank control group, && P ＜0.01, &&&& P ＜0.0001 versus the icariin group. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

    Techniques Used: Inhibition, Concentration Assay, CCK-8 Assay, Staining

    BMP/Smad4 signalling pathway altered in Eno1-regulated osteogenic differentiation. (A) Western Blot analysis for BMP4, BMP2, Smad4, p-Smad1/5/9 and Smad1/5/9 were performed. Vinculin was used as a reference protein. Relative expression of BMP4 (B), BMP2 (C) and Smad4 (D) were normalized against Vinculin. (E)The ratio of p-Smad1/5/9 and Smad1/5/9 was displayed. All the data are shown as mean ± SD (n = 3) in three independent experiments. * P ＜0.05, ** P ＜0.01versus the blank control group, && P ＜0.01, &&& P ＜0.001 versus the icariin group.
    Figure Legend Snippet: BMP/Smad4 signalling pathway altered in Eno1-regulated osteogenic differentiation. (A) Western Blot analysis for BMP4, BMP2, Smad4, p-Smad1/5/9 and Smad1/5/9 were performed. Vinculin was used as a reference protein. Relative expression of BMP4 (B), BMP2 (C) and Smad4 (D) were normalized against Vinculin. (E)The ratio of p-Smad1/5/9 and Smad1/5/9 was displayed. All the data are shown as mean ± SD (n = 3) in three independent experiments. * P ＜0.05, ** P ＜0.01versus the blank control group, && P ＜0.01, &&& P ＜0.001 versus the icariin group.

    Techniques Used: Western Blot, Expressing

    eno1  (Abcam)

     
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    Abcam eno1
    A GSEA result of RNA-seq of BLCA cells after 24 h melatonin (0 mM, 1 mM, 2 mM, and 4 mM) treatment. B Detection of cellular pyruvate level after 24 h melatonin treatment in BLCA cells ( n = 3). C Heatmap of the alteration of glycolytic enzymes in BLCA cells after 24 h melatonin (0 mM, 1 mM, 2 mM, and 4 mM) treatment. D Venn map of co-DEGs in GSE3167, GSE7476, GSE27488, and glycolysis enzymes. E Expression level of <t>ENO1</t> in normal bladder tissues versus BLCA tissues in GSE13507 dataset. F Expression level of ENO1 in low-grade BLCA tissues versus high-grade BLCA tissues in GSE13507 dataset. G Expression level of ENO1 in BLCA tissues with or without progression in GSE13507 dataset. H Survival analysis of BLCA patients with different ENO1 mRNA level in GSE13507 dataset. I qRT-PCR analysis of ENO1 expression alteration after 24 h melatonin (0 mM, 1 mM, 2 mM, and 4 mM) treatment in BLCA cells ( n = 4). J Western blot assay of ENO1 protein alteration after 24 h melatonin (0 mM, 1 mM, 2 mM, and 4 mM) treatment in BLCA cells. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Eno1, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    eno1 - by Bioz Stars, 2023-10
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    1) Product Images from "Melatonin inhibits bladder tumorigenesis by suppressing PPARγ/ENO1-mediated glycolysis"

    Article Title: Melatonin inhibits bladder tumorigenesis by suppressing PPARγ/ENO1-mediated glycolysis

    Journal: Cell Death & Disease

    doi: 10.1038/s41419-023-05770-8

    A GSEA result of RNA-seq of BLCA cells after 24 h melatonin (0 mM, 1 mM, 2 mM, and 4 mM) treatment. B Detection of cellular pyruvate level after 24 h melatonin treatment in BLCA cells ( n = 3). C Heatmap of the alteration of glycolytic enzymes in BLCA cells after 24 h melatonin (0 mM, 1 mM, 2 mM, and 4 mM) treatment. D Venn map of co-DEGs in GSE3167, GSE7476, GSE27488, and glycolysis enzymes. E Expression level of ENO1 in normal bladder tissues versus BLCA tissues in GSE13507 dataset. F Expression level of ENO1 in low-grade BLCA tissues versus high-grade BLCA tissues in GSE13507 dataset. G Expression level of ENO1 in BLCA tissues with or without progression in GSE13507 dataset. H Survival analysis of BLCA patients with different ENO1 mRNA level in GSE13507 dataset. I qRT-PCR analysis of ENO1 expression alteration after 24 h melatonin (0 mM, 1 mM, 2 mM, and 4 mM) treatment in BLCA cells ( n = 4). J Western blot assay of ENO1 protein alteration after 24 h melatonin (0 mM, 1 mM, 2 mM, and 4 mM) treatment in BLCA cells. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: A GSEA result of RNA-seq of BLCA cells after 24 h melatonin (0 mM, 1 mM, 2 mM, and 4 mM) treatment. B Detection of cellular pyruvate level after 24 h melatonin treatment in BLCA cells ( n = 3). C Heatmap of the alteration of glycolytic enzymes in BLCA cells after 24 h melatonin (0 mM, 1 mM, 2 mM, and 4 mM) treatment. D Venn map of co-DEGs in GSE3167, GSE7476, GSE27488, and glycolysis enzymes. E Expression level of ENO1 in normal bladder tissues versus BLCA tissues in GSE13507 dataset. F Expression level of ENO1 in low-grade BLCA tissues versus high-grade BLCA tissues in GSE13507 dataset. G Expression level of ENO1 in BLCA tissues with or without progression in GSE13507 dataset. H Survival analysis of BLCA patients with different ENO1 mRNA level in GSE13507 dataset. I qRT-PCR analysis of ENO1 expression alteration after 24 h melatonin (0 mM, 1 mM, 2 mM, and 4 mM) treatment in BLCA cells ( n = 4). J Western blot assay of ENO1 protein alteration after 24 h melatonin (0 mM, 1 mM, 2 mM, and 4 mM) treatment in BLCA cells. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: RNA Sequencing Assay, Expressing, Quantitative RT-PCR, Western Blot

    Clinicopathological statistics of BLCA patients from GSE13507 based on ENO1 expression level.
    Figure Legend Snippet: Clinicopathological statistics of BLCA patients from GSE13507 based on ENO1 expression level.

    Techniques Used: Expressing

    A IC50 value of 24 h melatonin treatment on UM-UC3 cells with exogenous pyruvate (3 mM) supplement ( n = 3). B Statistical analysis of clone formation assay of UM-UC3 cells under 48 h melatonin (2 mM) treatment and exogenous pyruvate (3 mM) supplement ( n = 3). C Statistical analysis of apoptotic cells of UM-UC3 cells after 24 h melatonin (2 mM) treatment with exogenous pyruvate (3 mM) supplement ( n = 3). D Western blot assay of apoptosis-related proteins of UM-UC3 cells after 24 h melatonin (2 mM) treatment with exogenous pyruvate (3 mM) supplement. E MTT assay of UM-UC3 cells after silencing ENO1 with exogenous pyruvate (3 mM) supplement ( n = 3), negative control siRNA was added. F Statistical analysis of clone formation assay of UM-UC3 cells after silencing ENO1 with exogenous pyruvate (3 mM) supplement ( n = 3), negative control siRNA was added in “-” of siE-1 group. G Statistical analysis of apoptotic cells of UM-UC3 cells after silencing ENO1 with exogenous pyruvate (3 mM) supplement ( n = 3), negative control siRNA was added in “-” of siE-1 group. H Western blot assay of apoptosis-related proteins of UM-UC3 cells after silencing ENO1 with exogenous pyruvate (3 mM) supplement, negative control siRNA was added in “-” of siE-1 group. I Statistical analysis of transwell assay of UM-UC3 cells after 24 h melatonin (2 mM) treatment with exogenous pyruvate (3 mM) supplement and statistical analysis ( n = 3). J Western blot assay of EMT-related proteins of UM-UC3 cells after 24 h melatonin (2 mM) treatment with exogenous pyruvate (3 mM) supplement. K Statistical analysis of transwell assay of UM-UC3 cells after silencing ENO1 with exogenous pyruvate (3 mM) supplement ( n = 3), negative control siRNA was added in “-” of siE-1 group. L Western blot assay of EMT-related proteins of UM-UC3 cells after silencing ENO1 with exogenous pyruvate (3 mM) supplement, negative control siRNA was added in “-” of siE-1 group. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: A IC50 value of 24 h melatonin treatment on UM-UC3 cells with exogenous pyruvate (3 mM) supplement ( n = 3). B Statistical analysis of clone formation assay of UM-UC3 cells under 48 h melatonin (2 mM) treatment and exogenous pyruvate (3 mM) supplement ( n = 3). C Statistical analysis of apoptotic cells of UM-UC3 cells after 24 h melatonin (2 mM) treatment with exogenous pyruvate (3 mM) supplement ( n = 3). D Western blot assay of apoptosis-related proteins of UM-UC3 cells after 24 h melatonin (2 mM) treatment with exogenous pyruvate (3 mM) supplement. E MTT assay of UM-UC3 cells after silencing ENO1 with exogenous pyruvate (3 mM) supplement ( n = 3), negative control siRNA was added. F Statistical analysis of clone formation assay of UM-UC3 cells after silencing ENO1 with exogenous pyruvate (3 mM) supplement ( n = 3), negative control siRNA was added in “-” of siE-1 group. G Statistical analysis of apoptotic cells of UM-UC3 cells after silencing ENO1 with exogenous pyruvate (3 mM) supplement ( n = 3), negative control siRNA was added in “-” of siE-1 group. H Western blot assay of apoptosis-related proteins of UM-UC3 cells after silencing ENO1 with exogenous pyruvate (3 mM) supplement, negative control siRNA was added in “-” of siE-1 group. I Statistical analysis of transwell assay of UM-UC3 cells after 24 h melatonin (2 mM) treatment with exogenous pyruvate (3 mM) supplement and statistical analysis ( n = 3). J Western blot assay of EMT-related proteins of UM-UC3 cells after 24 h melatonin (2 mM) treatment with exogenous pyruvate (3 mM) supplement. K Statistical analysis of transwell assay of UM-UC3 cells after silencing ENO1 with exogenous pyruvate (3 mM) supplement ( n = 3), negative control siRNA was added in “-” of siE-1 group. L Western blot assay of EMT-related proteins of UM-UC3 cells after silencing ENO1 with exogenous pyruvate (3 mM) supplement, negative control siRNA was added in “-” of siE-1 group. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Tube Formation Assay, Western Blot, MTT Assay, Negative Control, Transwell Assay

    A – B Expression status of glycolysis enzymes in GSE77883. C IC50 value of gemcitabine on BLCA cells with different culture conditions under 48 h culture ( n = 3), negative control siRNA was added. D Statistical analysis of apoptotic cells of UM-UC3 cells after 48 h gemcitabine (0.5 μM) treatment with exogenous pyruvate (3 mM) supplement ( n = 3). E Western blot assay of γH2AX alteration in UM-UC3 cells with 48 h gemcitabine (0.5 μM) treatment and 3 mM pyruvate supplement. F Statistical analysis of apoptotic cells of UM-UC3 cells with 48 h gemcitabine (0.5 μM) treatment and 24 h 2 mM melatonin treatment ( n = 4). G Western blot assay of γH2AX alteration in UM-UC3 cells with 48 h gemcitabine (0.5 μM) treatment and 24 h 2 mM melatonin treatment. H Statistical analysis of apoptotic cells of UM-UC3 cells with 48 h gemcitabine (0.5 μM) treatment and silencing ENO1 ( n = 3), negative control siRNA was added in “-” of siE-1 group. I Western blot assay of γH2AX alteration in UM-UC3 cells with 48 h gemcitabine (0.5 μM) treatment and silencing ENO1 , negative control siRNA was added in “-” of siE-1 group. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: A – B Expression status of glycolysis enzymes in GSE77883. C IC50 value of gemcitabine on BLCA cells with different culture conditions under 48 h culture ( n = 3), negative control siRNA was added. D Statistical analysis of apoptotic cells of UM-UC3 cells after 48 h gemcitabine (0.5 μM) treatment with exogenous pyruvate (3 mM) supplement ( n = 3). E Western blot assay of γH2AX alteration in UM-UC3 cells with 48 h gemcitabine (0.5 μM) treatment and 3 mM pyruvate supplement. F Statistical analysis of apoptotic cells of UM-UC3 cells with 48 h gemcitabine (0.5 μM) treatment and 24 h 2 mM melatonin treatment ( n = 4). G Western blot assay of γH2AX alteration in UM-UC3 cells with 48 h gemcitabine (0.5 μM) treatment and 24 h 2 mM melatonin treatment. H Statistical analysis of apoptotic cells of UM-UC3 cells with 48 h gemcitabine (0.5 μM) treatment and silencing ENO1 ( n = 3), negative control siRNA was added in “-” of siE-1 group. I Western blot assay of γH2AX alteration in UM-UC3 cells with 48 h gemcitabine (0.5 μM) treatment and silencing ENO1 , negative control siRNA was added in “-” of siE-1 group. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Expressing, Negative Control, Western Blot

    A Western blot results of PPARγ protein alteration with 24 h melatonin treatment. B Spearman correlation analysis of the expression level of ENO1 and PPARγ in GSE3167. C The binding site of PPARγ obtained from the JASPAR database. D ChIP-seq data of esophageal adenocarcinoma showing the binding of PPARγ on ENO1 promoter region. E qRT-PCR results of ENO1 mRNA level with GW9662 treatment in T24 cells ( n = 3). F Western blot results of ENO1 protein level with PPARγ overexpression and melatonin (4 mM) treatment, empty vector was added. G Pattern of dual-luciferase reporter construction and ChIP-qRT-PCR primer design. H Dual-luciferase reporter assay of ENO1 promoter activity ( n = 3). I ChIP-qPCR assay of putative PPARγ binding sites on ENO1 promoter ( n = 3). J Statistical analysis of clone formation assay of 5637 cells and UM-UC3 cells ( n = 3), empty vector or negative control siRNA was added. * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: A Western blot results of PPARγ protein alteration with 24 h melatonin treatment. B Spearman correlation analysis of the expression level of ENO1 and PPARγ in GSE3167. C The binding site of PPARγ obtained from the JASPAR database. D ChIP-seq data of esophageal adenocarcinoma showing the binding of PPARγ on ENO1 promoter region. E qRT-PCR results of ENO1 mRNA level with GW9662 treatment in T24 cells ( n = 3). F Western blot results of ENO1 protein level with PPARγ overexpression and melatonin (4 mM) treatment, empty vector was added. G Pattern of dual-luciferase reporter construction and ChIP-qRT-PCR primer design. H Dual-luciferase reporter assay of ENO1 promoter activity ( n = 3). I ChIP-qPCR assay of putative PPARγ binding sites on ENO1 promoter ( n = 3). J Statistical analysis of clone formation assay of 5637 cells and UM-UC3 cells ( n = 3), empty vector or negative control siRNA was added. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Western Blot, Expressing, Binding Assay, ChIP-sequencing, Quantitative RT-PCR, Over Expression, Plasmid Preparation, Luciferase, Reporter Assay, Activity Assay, Tube Formation Assay, Negative Control

    Left panel: without melatonin treatment, PPARγ promotes ENO1 transcription to complete the integral glycolysis process, and the mitochondrion function normally to maintain cellular redox homeostasis. Right panel: under melatonin treatment, melatonin inhibits PPARγ-ENO1-mediated glycolysis. Decreased pyruvate production causes increased mitochondrion burden leading to abnormal ROS accumulation.
    Figure Legend Snippet: Left panel: without melatonin treatment, PPARγ promotes ENO1 transcription to complete the integral glycolysis process, and the mitochondrion function normally to maintain cellular redox homeostasis. Right panel: under melatonin treatment, melatonin inhibits PPARγ-ENO1-mediated glycolysis. Decreased pyruvate production causes increased mitochondrion burden leading to abnormal ROS accumulation.

    Techniques Used:

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    • rabbit monoclonal eno1  (Abcam)
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    Abcam rabbit monoclonal eno1
    Source, application and concentration of antibodies.
    Rabbit Monoclonal Eno1, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti eno1 2 3 ab189891 antibodies  (Abcam)
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    Source, application and concentration of antibodies.
    Anti Eno1 2 3 Ab189891 Antibodies, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    eno1 antibodies  (Abcam)
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    Abcam eno1 antibodies
    The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between <t>ENO1,</t> GRN, and PTGS2 with immune infiltrating cells.
    Eno1 Antibodies, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    eno1  (Abcam)
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    The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between <t>ENO1,</t> GRN, and PTGS2 with immune infiltrating cells.
    Eno1, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rabbitanti eno1 antibodies  (Abcam)
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    The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between <t>ENO1,</t> GRN, and PTGS2 with immune infiltrating cells.
    Rabbitanti Eno1 Antibodies, supplied by Abcam, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    eno1 antibody  (Abcam)
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    Abcam eno1 antibody
    Characterization of the <t>ENO1</t> -RNA interaction profile by an iRIP-seq analysis. (A) Experimental and computational work flow of the iRIP-seq. (B) Western blot analysis of the ENO1 immunoprecipitates using anti-Flag monoclonal antibody. Two replicates were performed. (C) Sample cluster analysis plots. (D) Sample correlation analysis. (E) A pie chart showing the genomic distribution of the ENO1 -bound peaks from the two biological replicates. (F) The motif analysis results showing the enriched motifs from the ENO1 -bound peaks from the two biological replicates. (G) The distribution of the GACGAGGA enrichment sequences in both experiments in the Ablife analysis. (H) A Venn diagram showing the overlapping peaks between IP-1 and IP-2. (I) A scatter plot showing the most enriched GO biological process (left panel) and KEGG pathway (right panel) results of the overlapping peak genes. ENO1 , enolase 1; IgG, immunoglobulin G; RT-PCR, reverse transcription-polymerase chain reaction; IP, immunoprecipitation; PPIA, peptidylprolyl isomerase A; 3'UTR, 3' untranslated region; 5'UTR, 5' untranslated region; CDS, coding sequence; nc, non-coding; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; iRIP-seq, improved RNA immunoprecipitation and deep sequencing.
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    Source, application and concentration of antibodies.

    Journal: PLOS ONE

    Article Title: Helicase-like transcription factor (HLTF) -deleted CDX/TME model of colorectal cancer increased transcription of oxidative phosphorylation genes and diverted glycolysis to boost S-glutathionylation in lymphatic intravascular metastatic niches

    doi: 10.1371/journal.pone.0291023

    Figure Lengend Snippet: Source, application and concentration of antibodies.

    Article Snippet: Rabbit polyclonal HLTF antibody (NBP1-83256) Novus Biologicals (1:100) Rabbit polyclonal CYTB (55090-1-AP) ThermoFisher Scientific (1:50) Rabbit polyclonal PGAM1 (16126-1-AP) ThermoFisher Scientific (1:50) Rabbit polyclonal ANXA1 (71–3400) ThermoFisher Scientific (1:20) Rabbit monoclonal γH2AX-phospho S139 (ab81299) Abcam (1:50) Rabbit monoclonal ENO1 (ab227978) Abcam (1:2,000) Rabbit recombinant monoclonal mouse-specific PDPN (MA5-29742) ThermoFisher Scientific (1:500) , IHC-P: Vector Laboratories RTU Biotinylated Goat Anti-rabbit IgG (H+L) (BP-9100-50).

    Techniques: Concentration Assay, Recombinant, Plasmid Preparation

    Summary of site-specific S-glutathionylation identified by 2D-DIGE MALDI-TOF/TOF mass spectrometry. Pr-SSG in HLTF -/- CDX/TME.

    Journal: PLOS ONE

    Article Title: Helicase-like transcription factor (HLTF) -deleted CDX/TME model of colorectal cancer increased transcription of oxidative phosphorylation genes and diverted glycolysis to boost S-glutathionylation in lymphatic intravascular metastatic niches

    doi: 10.1371/journal.pone.0291023

    Figure Lengend Snippet: Summary of site-specific S-glutathionylation identified by 2D-DIGE MALDI-TOF/TOF mass spectrometry. Pr-SSG in HLTF -/- CDX/TME.

    Article Snippet: Rabbit polyclonal HLTF antibody (NBP1-83256) Novus Biologicals (1:100) Rabbit polyclonal CYTB (55090-1-AP) ThermoFisher Scientific (1:50) Rabbit polyclonal PGAM1 (16126-1-AP) ThermoFisher Scientific (1:50) Rabbit polyclonal ANXA1 (71–3400) ThermoFisher Scientific (1:20) Rabbit monoclonal γH2AX-phospho S139 (ab81299) Abcam (1:50) Rabbit monoclonal ENO1 (ab227978) Abcam (1:2,000) Rabbit recombinant monoclonal mouse-specific PDPN (MA5-29742) ThermoFisher Scientific (1:500) , IHC-P: Vector Laboratories RTU Biotinylated Goat Anti-rabbit IgG (H+L) (BP-9100-50).

    Techniques: Mass Spectrometry

    The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between ENO1, GRN, and PTGS2 with immune infiltrating cells.

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between ENO1, GRN, and PTGS2 with immune infiltrating cells.

    Article Snippet: Protein was electrophoresed with SDS-PAGE gel and transferred to PVDF membrane, blocked using QuickBlock™ Primary Antibody Dilution Buffer (Beyotime, China), and then incubated with the ENO1 antibodies (ab227978, Abcam), GRN antibodies (DF7997, Affinity Biosciences), PTGS2 antibodies (K001561P, Solarbio) and ACSL4 (ab155282, Abcam) at 4°C overnight.

    Techniques:

    GWAS analysis to identify the pathogenic regions of the hub genes. The Manhattan plot shows the SNP pathogenic regions corresponding to PTGS2, ENO1 and GRN.

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: GWAS analysis to identify the pathogenic regions of the hub genes. The Manhattan plot shows the SNP pathogenic regions corresponding to PTGS2, ENO1 and GRN.

    Article Snippet: Protein was electrophoresed with SDS-PAGE gel and transferred to PVDF membrane, blocked using QuickBlock™ Primary Antibody Dilution Buffer (Beyotime, China), and then incubated with the ENO1 antibodies (ab227978, Abcam), GRN antibodies (DF7997, Affinity Biosciences), PTGS2 antibodies (K001561P, Solarbio) and ACSL4 (ab155282, Abcam) at 4°C overnight.

    Techniques:

    GSEA analysis of hub genes. (A) The top 3 most enriched pathways about function enrichment of PTGS2 gene: Nod-like receptor signaling pathway, gene set enriched in FcγR mediated phagocytosis, gene set enriched in the Chemokine signaling pathway. (B) The top 3 most enriched pathways about function enrichment of GRN gene: Lysosome, Leishmania infection, B cell receptor signaling pathway. (C) The top 3 most enriched pathways about function enrichment of ENO1 gene: Lysosome, Pathogenic Escherichia coli infection, Leishmania infection. Screening criteria for significant gene sets included adj. p-value < 0.05 and FDR < 0.5. NES, normalized enrichment score.

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: GSEA analysis of hub genes. (A) The top 3 most enriched pathways about function enrichment of PTGS2 gene: Nod-like receptor signaling pathway, gene set enriched in FcγR mediated phagocytosis, gene set enriched in the Chemokine signaling pathway. (B) The top 3 most enriched pathways about function enrichment of GRN gene: Lysosome, Leishmania infection, B cell receptor signaling pathway. (C) The top 3 most enriched pathways about function enrichment of ENO1 gene: Lysosome, Pathogenic Escherichia coli infection, Leishmania infection. Screening criteria for significant gene sets included adj. p-value < 0.05 and FDR < 0.5. NES, normalized enrichment score.

    Article Snippet: Protein was electrophoresed with SDS-PAGE gel and transferred to PVDF membrane, blocked using QuickBlock™ Primary Antibody Dilution Buffer (Beyotime, China), and then incubated with the ENO1 antibodies (ab227978, Abcam), GRN antibodies (DF7997, Affinity Biosciences), PTGS2 antibodies (K001561P, Solarbio) and ACSL4 (ab155282, Abcam) at 4°C overnight.

    Techniques: Infection

    Enrichment analysis for transcription factors of hub genes (A) Histogram of the AUC. By calculating the AUC, the over-representation of each motif for hub genes was assessed. Red vertical line indicates the degree of significance, whereby motifs with AUC higher than the significance level are considered significant motifs. (B) The recovery curve for the three most significant motifs. Red line represents the global mean of recovered motif curve, green line represents the mean ± standard deviation. Motifs that were larger than the mean ± standard deviation were considered statistically significant. Blue line represents the current motif’s recovered curve. The motif cisbp_M5493 was significantly enriched in hub genes (ENO1 and PTGS2).

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: Enrichment analysis for transcription factors of hub genes (A) Histogram of the AUC. By calculating the AUC, the over-representation of each motif for hub genes was assessed. Red vertical line indicates the degree of significance, whereby motifs with AUC higher than the significance level are considered significant motifs. (B) The recovery curve for the three most significant motifs. Red line represents the global mean of recovered motif curve, green line represents the mean ± standard deviation. Motifs that were larger than the mean ± standard deviation were considered statistically significant. Blue line represents the current motif’s recovered curve. The motif cisbp_M5493 was significantly enriched in hub genes (ENO1 and PTGS2).

    Article Snippet: Protein was electrophoresed with SDS-PAGE gel and transferred to PVDF membrane, blocked using QuickBlock™ Primary Antibody Dilution Buffer (Beyotime, China), and then incubated with the ENO1 antibodies (ab227978, Abcam), GRN antibodies (DF7997, Affinity Biosciences), PTGS2 antibodies (K001561P, Solarbio) and ACSL4 (ab155282, Abcam) at 4°C overnight.

    Techniques: Standard Deviation

    Single-cell analysis revealed the expression of PTGS2, ENO1 and GRN. (A) Dot plot of hub genes for each cell type. (B) Violin plots showing the expression level of hub genes in nine cell type.

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: Single-cell analysis revealed the expression of PTGS2, ENO1 and GRN. (A) Dot plot of hub genes for each cell type. (B) Violin plots showing the expression level of hub genes in nine cell type.

    Article Snippet: Protein was electrophoresed with SDS-PAGE gel and transferred to PVDF membrane, blocked using QuickBlock™ Primary Antibody Dilution Buffer (Beyotime, China), and then incubated with the ENO1 antibodies (ab227978, Abcam), GRN antibodies (DF7997, Affinity Biosciences), PTGS2 antibodies (K001561P, Solarbio) and ACSL4 (ab155282, Abcam) at 4°C overnight.

    Techniques: Single-cell Analysis, Expressing

    Validation of the hub genes in experimental samples. (A) Representative tracing of the PI and the joint swelling thickness in rat after CFA or Nor treatment in the two groups(n=12). (B) Representative images of H&E staining of joint sections from AIA rat or Nor rat. (C) The expression of GRN, PTGS2 and ENO1. n = 3. *p < 0.05, **p < 0.01, ***p < 0.001. (D) IHC staining for PTGS2, ENO1, and GRN on synovium from samples of OA and RA patients (n = 3).

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: Validation of the hub genes in experimental samples. (A) Representative tracing of the PI and the joint swelling thickness in rat after CFA or Nor treatment in the two groups(n=12). (B) Representative images of H&E staining of joint sections from AIA rat or Nor rat. (C) The expression of GRN, PTGS2 and ENO1. n = 3. *p < 0.05, **p < 0.01, ***p < 0.001. (D) IHC staining for PTGS2, ENO1, and GRN on synovium from samples of OA and RA patients (n = 3).

    Article Snippet: Protein was electrophoresed with SDS-PAGE gel and transferred to PVDF membrane, blocked using QuickBlock™ Primary Antibody Dilution Buffer (Beyotime, China), and then incubated with the ENO1 antibodies (ab227978, Abcam), GRN antibodies (DF7997, Affinity Biosciences), PTGS2 antibodies (K001561P, Solarbio) and ACSL4 (ab155282, Abcam) at 4°C overnight.

    Techniques: Staining, Expressing, Immunohistochemistry

    (A) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model with knockdown of ENO1-siRNA (n=3). (B) The expression level of ENO1 and ACO1 in primary FLS of RA patients(n=3). (C, D) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model and RA patients with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/) (n=3). (E) The assessment of cell viability by CCK-8 assay in primary FLS of rat models with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ### P < 0.001 versus siRNA group. ****P < 0.0001 versus siRNA group; #P < 0.05 and ## P < 0.01 versus siRNA+Fe2+group. (F) The assessment of cell viability by CCK-8 assay in primary FLS of RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ###P < 0.001 versus siRNA group. *P < 0.05 versus siRNA group; # P < 0.05 versus siRNA+Fe 2+ group.

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: (A) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model with knockdown of ENO1-siRNA (n=3). (B) The expression level of ENO1 and ACO1 in primary FLS of RA patients(n=3). (C, D) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model and RA patients with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/) (n=3). (E) The assessment of cell viability by CCK-8 assay in primary FLS of rat models with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ### P < 0.001 versus siRNA group. ****P < 0.0001 versus siRNA group; #P < 0.05 and ## P < 0.01 versus siRNA+Fe2+group. (F) The assessment of cell viability by CCK-8 assay in primary FLS of RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ###P < 0.001 versus siRNA group. *P < 0.05 versus siRNA group; # P < 0.05 versus siRNA+Fe 2+ group.

    Article Snippet: Protein was electrophoresed with SDS-PAGE gel and transferred to PVDF membrane, blocked using QuickBlock™ Primary Antibody Dilution Buffer (Beyotime, China), and then incubated with the ENO1 antibodies (ab227978, Abcam), GRN antibodies (DF7997, Affinity Biosciences), PTGS2 antibodies (K001561P, Solarbio) and ACSL4 (ab155282, Abcam) at 4°C overnight.

    Techniques: Expressing, CCK-8 Assay

    The assessment of lipid peroxidation by flow cytometry in primary FLS of rat model (A) and RA patients (B) with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). (C) The assessment of Intracellular ferrous ion by cellular ferrous ion detection fluorescent probes in primary FLS of rat model and RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/).

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: The assessment of lipid peroxidation by flow cytometry in primary FLS of rat model (A) and RA patients (B) with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). (C) The assessment of Intracellular ferrous ion by cellular ferrous ion detection fluorescent probes in primary FLS of rat model and RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/).

    Article Snippet: Protein was electrophoresed with SDS-PAGE gel and transferred to PVDF membrane, blocked using QuickBlock™ Primary Antibody Dilution Buffer (Beyotime, China), and then incubated with the ENO1 antibodies (ab227978, Abcam), GRN antibodies (DF7997, Affinity Biosciences), PTGS2 antibodies (K001561P, Solarbio) and ACSL4 (ab155282, Abcam) at 4°C overnight.

    Techniques: Flow Cytometry

    The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between ENO1, GRN, and PTGS2 with immune infiltrating cells.

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: The landscape of immune infiltration between the normal and RA group. (A) Cumulative histogram showing the relative percentages of 22 different immune cell types. (B) Violin plot shows the comparisons between immune cells in normal controls and RA patients. (C) The heatmap shows the correlation in the infiltration of 22 immune cell type proportions. (D-F) Correlation between ENO1, GRN, and PTGS2 with immune infiltrating cells.

    Article Snippet: Sections were immersed with antibodies against PTGS2(1:200, K001561P, Solarbio), ENO1(1:200, ab227978, Abcam), GRN (1:200, DF7997, Affinity Biosciences) overnight at 4°C.

    Techniques:

    GWAS analysis to identify the pathogenic regions of the hub genes. The Manhattan plot shows the SNP pathogenic regions corresponding to PTGS2, ENO1 and GRN.

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: GWAS analysis to identify the pathogenic regions of the hub genes. The Manhattan plot shows the SNP pathogenic regions corresponding to PTGS2, ENO1 and GRN.

    Article Snippet: Sections were immersed with antibodies against PTGS2(1:200, K001561P, Solarbio), ENO1(1:200, ab227978, Abcam), GRN (1:200, DF7997, Affinity Biosciences) overnight at 4°C.

    Techniques:

    GSEA analysis of hub genes. (A) The top 3 most enriched pathways about function enrichment of PTGS2 gene: Nod-like receptor signaling pathway, gene set enriched in FcγR mediated phagocytosis, gene set enriched in the Chemokine signaling pathway. (B) The top 3 most enriched pathways about function enrichment of GRN gene: Lysosome, Leishmania infection, B cell receptor signaling pathway. (C) The top 3 most enriched pathways about function enrichment of ENO1 gene: Lysosome, Pathogenic Escherichia coli infection, Leishmania infection. Screening criteria for significant gene sets included adj. p-value < 0.05 and FDR < 0.5. NES, normalized enrichment score.

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: GSEA analysis of hub genes. (A) The top 3 most enriched pathways about function enrichment of PTGS2 gene: Nod-like receptor signaling pathway, gene set enriched in FcγR mediated phagocytosis, gene set enriched in the Chemokine signaling pathway. (B) The top 3 most enriched pathways about function enrichment of GRN gene: Lysosome, Leishmania infection, B cell receptor signaling pathway. (C) The top 3 most enriched pathways about function enrichment of ENO1 gene: Lysosome, Pathogenic Escherichia coli infection, Leishmania infection. Screening criteria for significant gene sets included adj. p-value < 0.05 and FDR < 0.5. NES, normalized enrichment score.

    Article Snippet: Sections were immersed with antibodies against PTGS2(1:200, K001561P, Solarbio), ENO1(1:200, ab227978, Abcam), GRN (1:200, DF7997, Affinity Biosciences) overnight at 4°C.

    Techniques: Infection

    Enrichment analysis for transcription factors of hub genes (A) Histogram of the AUC. By calculating the AUC, the over-representation of each motif for hub genes was assessed. Red vertical line indicates the degree of significance, whereby motifs with AUC higher than the significance level are considered significant motifs. (B) The recovery curve for the three most significant motifs. Red line represents the global mean of recovered motif curve, green line represents the mean ± standard deviation. Motifs that were larger than the mean ± standard deviation were considered statistically significant. Blue line represents the current motif’s recovered curve. The motif cisbp_M5493 was significantly enriched in hub genes (ENO1 and PTGS2).

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: Enrichment analysis for transcription factors of hub genes (A) Histogram of the AUC. By calculating the AUC, the over-representation of each motif for hub genes was assessed. Red vertical line indicates the degree of significance, whereby motifs with AUC higher than the significance level are considered significant motifs. (B) The recovery curve for the three most significant motifs. Red line represents the global mean of recovered motif curve, green line represents the mean ± standard deviation. Motifs that were larger than the mean ± standard deviation were considered statistically significant. Blue line represents the current motif’s recovered curve. The motif cisbp_M5493 was significantly enriched in hub genes (ENO1 and PTGS2).

    Article Snippet: Sections were immersed with antibodies against PTGS2(1:200, K001561P, Solarbio), ENO1(1:200, ab227978, Abcam), GRN (1:200, DF7997, Affinity Biosciences) overnight at 4°C.

    Techniques: Standard Deviation

    Single-cell analysis revealed the expression of PTGS2, ENO1 and GRN. (A) Dot plot of hub genes for each cell type. (B) Violin plots showing the expression level of hub genes in nine cell type.

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: Single-cell analysis revealed the expression of PTGS2, ENO1 and GRN. (A) Dot plot of hub genes for each cell type. (B) Violin plots showing the expression level of hub genes in nine cell type.

    Article Snippet: Sections were immersed with antibodies against PTGS2(1:200, K001561P, Solarbio), ENO1(1:200, ab227978, Abcam), GRN (1:200, DF7997, Affinity Biosciences) overnight at 4°C.

    Techniques: Single-cell Analysis, Expressing

    Validation of the hub genes in experimental samples. (A) Representative tracing of the PI and the joint swelling thickness in rat after CFA or Nor treatment in the two groups(n=12). (B) Representative images of H&E staining of joint sections from AIA rat or Nor rat. (C) The expression of GRN, PTGS2 and ENO1. n = 3. *p < 0.05, **p < 0.01, ***p < 0.001. (D) IHC staining for PTGS2, ENO1, and GRN on synovium from samples of OA and RA patients (n = 3).

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: Validation of the hub genes in experimental samples. (A) Representative tracing of the PI and the joint swelling thickness in rat after CFA or Nor treatment in the two groups(n=12). (B) Representative images of H&E staining of joint sections from AIA rat or Nor rat. (C) The expression of GRN, PTGS2 and ENO1. n = 3. *p < 0.05, **p < 0.01, ***p < 0.001. (D) IHC staining for PTGS2, ENO1, and GRN on synovium from samples of OA and RA patients (n = 3).

    Article Snippet: Sections were immersed with antibodies against PTGS2(1:200, K001561P, Solarbio), ENO1(1:200, ab227978, Abcam), GRN (1:200, DF7997, Affinity Biosciences) overnight at 4°C.

    Techniques: Staining, Expressing, Immunohistochemistry

    (A) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model with knockdown of ENO1-siRNA (n=3). (B) The expression level of ENO1 and ACO1 in primary FLS of RA patients(n=3). (C, D) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model and RA patients with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/) (n=3). (E) The assessment of cell viability by CCK-8 assay in primary FLS of rat models with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ### P < 0.001 versus siRNA group. ****P < 0.0001 versus siRNA group; #P < 0.05 and ## P < 0.01 versus siRNA+Fe2+group. (F) The assessment of cell viability by CCK-8 assay in primary FLS of RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ###P < 0.001 versus siRNA group. *P < 0.05 versus siRNA group; # P < 0.05 versus siRNA+Fe 2+ group.

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: (A) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model with knockdown of ENO1-siRNA (n=3). (B) The expression level of ENO1 and ACO1 in primary FLS of RA patients(n=3). (C, D) The expression level of ENO1, ACO1 and ACSL4 in primary FLS of rat model and RA patients with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/) (n=3). (E) The assessment of cell viability by CCK-8 assay in primary FLS of rat models with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ### P < 0.001 versus siRNA group. ****P < 0.0001 versus siRNA group; #P < 0.05 and ## P < 0.01 versus siRNA+Fe2+group. (F) The assessment of cell viability by CCK-8 assay in primary FLS of RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). Data are means ± SD. *P < 0.05 , ****P < 0.0001 and ns (no significance) versus RA group; ###P < 0.001 versus siRNA group. *P < 0.05 versus siRNA group; # P < 0.05 versus siRNA+Fe 2+ group.

    Article Snippet: Sections were immersed with antibodies against PTGS2(1:200, K001561P, Solarbio), ENO1(1:200, ab227978, Abcam), GRN (1:200, DF7997, Affinity Biosciences) overnight at 4°C.

    Techniques: Expressing, CCK-8 Assay

    The assessment of lipid peroxidation by flow cytometry in primary FLS of rat model (A) and RA patients (B) with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). (C) The assessment of Intracellular ferrous ion by cellular ferrous ion detection fluorescent probes in primary FLS of rat model and RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/).

    Journal: Frontiers in Immunology

    Article Title: Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

    doi: 10.3389/fimmu.2023.1197275

    Figure Lengend Snippet: The assessment of lipid peroxidation by flow cytometry in primary FLS of rat model (A) and RA patients (B) with knockdown of ENO1-siRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/). (C) The assessment of Intracellular ferrous ion by cellular ferrous ion detection fluorescent probes in primary FLS of rat model and RA patients with knockdown of ENO1-SiRNA in the presence of ferrous iron (200 μmol/L), Lip-1 (1 μmol/), Fer-1 (1 μmol/).

    Article Snippet: Sections were immersed with antibodies against PTGS2(1:200, K001561P, Solarbio), ENO1(1:200, ab227978, Abcam), GRN (1:200, DF7997, Affinity Biosciences) overnight at 4°C.

    Techniques: Flow Cytometry

    Characterization of the ENO1 -RNA interaction profile by an iRIP-seq analysis. (A) Experimental and computational work flow of the iRIP-seq. (B) Western blot analysis of the ENO1 immunoprecipitates using anti-Flag monoclonal antibody. Two replicates were performed. (C) Sample cluster analysis plots. (D) Sample correlation analysis. (E) A pie chart showing the genomic distribution of the ENO1 -bound peaks from the two biological replicates. (F) The motif analysis results showing the enriched motifs from the ENO1 -bound peaks from the two biological replicates. (G) The distribution of the GACGAGGA enrichment sequences in both experiments in the Ablife analysis. (H) A Venn diagram showing the overlapping peaks between IP-1 and IP-2. (I) A scatter plot showing the most enriched GO biological process (left panel) and KEGG pathway (right panel) results of the overlapping peak genes. ENO1 , enolase 1; IgG, immunoglobulin G; RT-PCR, reverse transcription-polymerase chain reaction; IP, immunoprecipitation; PPIA, peptidylprolyl isomerase A; 3'UTR, 3' untranslated region; 5'UTR, 5' untranslated region; CDS, coding sequence; nc, non-coding; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; iRIP-seq, improved RNA immunoprecipitation and deep sequencing.

    Journal: Journal of Gastrointestinal Oncology

    Article Title: RNA-binding protein ENO1 promotes the tumor progression of gastric cancer by binding to and regulating gastric cancer-related genes

    doi: 10.21037/jgo-23-151

    Figure Lengend Snippet: Characterization of the ENO1 -RNA interaction profile by an iRIP-seq analysis. (A) Experimental and computational work flow of the iRIP-seq. (B) Western blot analysis of the ENO1 immunoprecipitates using anti-Flag monoclonal antibody. Two replicates were performed. (C) Sample cluster analysis plots. (D) Sample correlation analysis. (E) A pie chart showing the genomic distribution of the ENO1 -bound peaks from the two biological replicates. (F) The motif analysis results showing the enriched motifs from the ENO1 -bound peaks from the two biological replicates. (G) The distribution of the GACGAGGA enrichment sequences in both experiments in the Ablife analysis. (H) A Venn diagram showing the overlapping peaks between IP-1 and IP-2. (I) A scatter plot showing the most enriched GO biological process (left panel) and KEGG pathway (right panel) results of the overlapping peak genes. ENO1 , enolase 1; IgG, immunoglobulin G; RT-PCR, reverse transcription-polymerase chain reaction; IP, immunoprecipitation; PPIA, peptidylprolyl isomerase A; 3'UTR, 3' untranslated region; 5'UTR, 5' untranslated region; CDS, coding sequence; nc, non-coding; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; iRIP-seq, improved RNA immunoprecipitation and deep sequencing.

    Article Snippet: ENO1 antibody was purchased from Abcam (Cambridge, UK).

    Techniques: Western Blot, Reverse Transcription Polymerase Chain Reaction, Immunoprecipitation, Sequencing

    ENO1 binds to genes related to the occurrence and development of GC. (A) The ENO1 -binding peak genes of NEAT1 . Left panel: an IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and red panels represent the positions of the peaks. The distribution reads of the bound gene are plotted in the upper panel and the transcripts of each gene are shown below. Right panel: a bar plot showing the FPKM of NEAT1 . (B) The ENO1 -binding peak genes of PKM . Left panel: an IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and blue panels represent the positions of the peaks. The distribution reads of the bound gene is plotted in the upper panel and the transcripts of each gene are shown below. Right panel: a bar plot showing the FPKM of PKM . (C) The ENO1 -binding peak genes of CD44 . Left panel: an IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and red panels represent the positions of the peaks. The distribution reads of the bound gene is plotted in the upper panel, and the transcripts of each gene are shown below. Right panel: a bar plot showing the FPKM of CD44 . **, P<0.05; ***, P<0.001. ENO1, enolase 1; IP, immunoprecipitation; NEAT1, nuclear enriched abundant transcript 1; PKM, pyruvate kinase M; GC, gastric cancer; IGV, Integrative Genomics Viewer; FPKM, fragments per kilobase million.

    Journal: Journal of Gastrointestinal Oncology

    Article Title: RNA-binding protein ENO1 promotes the tumor progression of gastric cancer by binding to and regulating gastric cancer-related genes

    doi: 10.21037/jgo-23-151

    Figure Lengend Snippet: ENO1 binds to genes related to the occurrence and development of GC. (A) The ENO1 -binding peak genes of NEAT1 . Left panel: an IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and red panels represent the positions of the peaks. The distribution reads of the bound gene are plotted in the upper panel and the transcripts of each gene are shown below. Right panel: a bar plot showing the FPKM of NEAT1 . (B) The ENO1 -binding peak genes of PKM . Left panel: an IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and blue panels represent the positions of the peaks. The distribution reads of the bound gene is plotted in the upper panel and the transcripts of each gene are shown below. Right panel: a bar plot showing the FPKM of PKM . (C) The ENO1 -binding peak genes of CD44 . Left panel: an IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and red panels represent the positions of the peaks. The distribution reads of the bound gene is plotted in the upper panel, and the transcripts of each gene are shown below. Right panel: a bar plot showing the FPKM of CD44 . **, P<0.05; ***, P<0.001. ENO1, enolase 1; IP, immunoprecipitation; NEAT1, nuclear enriched abundant transcript 1; PKM, pyruvate kinase M; GC, gastric cancer; IGV, Integrative Genomics Viewer; FPKM, fragments per kilobase million.

    Article Snippet: ENO1 antibody was purchased from Abcam (Cambridge, UK).

    Techniques: Binding Assay, Immunoprecipitation

    The ENO1 -interaction regulates the expression of the target genes associated with GC. The differentially expressed genes were output by using the data of previous gene chip sequencing. (A) Left panel: a Venn diagram showing the overlapping genes between the ENO1 -bound peaks in the fRIP-seq and the upregulated DEGs. Right panel: the overlapping genes between the ENO1 -bound peaks in the fRIP-seq and the downregulated DEGs. (B) A bar plot showing the expression pattern and statistical differences of the upregulated DEGs in the overlapping genes. The error bars represent the mean ± SEM. (C) A bar plot showing the expression pattern and statistical difference of the downregulated DEGs in the overlapping genes. The error bars represent the mean ± SEM. (D) The ENO1 -binding peak genes of MCL1 . An IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and blue panels represent the positions of the peaks. The read distribution of the bound gene is plotted in the upper panel and the transcripts of each gene are shown below. (E) The ENO1 -binding peak genes of SOX9 . An IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and blue panels represent the positions of the peaks. The read distribution of the bound gene is plotted in the upper panel and the transcripts of each gene are shown above. ***, P<0.001. DEG, differentially expressed gene; IP, immunoprecipitation; NC, negative control; KD, knockdown; MCL1, myeloid cell leukemia 1; VEGFA, vascular endothelial growth factor A; SOX9, SRY-box transcription factor 9; ENO1, enolase 1; GC, gastric cancer; fRIP-seq, formaldehyde crosslinking RNA immunoprecipitation sequencing; SEM, standard error of the mean; IGV, Integrative Genomics Viewer.

    Journal: Journal of Gastrointestinal Oncology

    Article Title: RNA-binding protein ENO1 promotes the tumor progression of gastric cancer by binding to and regulating gastric cancer-related genes

    doi: 10.21037/jgo-23-151

    Figure Lengend Snippet: The ENO1 -interaction regulates the expression of the target genes associated with GC. The differentially expressed genes were output by using the data of previous gene chip sequencing. (A) Left panel: a Venn diagram showing the overlapping genes between the ENO1 -bound peaks in the fRIP-seq and the upregulated DEGs. Right panel: the overlapping genes between the ENO1 -bound peaks in the fRIP-seq and the downregulated DEGs. (B) A bar plot showing the expression pattern and statistical differences of the upregulated DEGs in the overlapping genes. The error bars represent the mean ± SEM. (C) A bar plot showing the expression pattern and statistical difference of the downregulated DEGs in the overlapping genes. The error bars represent the mean ± SEM. (D) The ENO1 -binding peak genes of MCL1 . An IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and blue panels represent the positions of the peaks. The read distribution of the bound gene is plotted in the upper panel and the transcripts of each gene are shown below. (E) The ENO1 -binding peak genes of SOX9 . An IGV-sashimi plot showing the peak reads and binding sites across the mRNA; the green and blue panels represent the positions of the peaks. The read distribution of the bound gene is plotted in the upper panel and the transcripts of each gene are shown above. ***, P<0.001. DEG, differentially expressed gene; IP, immunoprecipitation; NC, negative control; KD, knockdown; MCL1, myeloid cell leukemia 1; VEGFA, vascular endothelial growth factor A; SOX9, SRY-box transcription factor 9; ENO1, enolase 1; GC, gastric cancer; fRIP-seq, formaldehyde crosslinking RNA immunoprecipitation sequencing; SEM, standard error of the mean; IGV, Integrative Genomics Viewer.

    Article Snippet: ENO1 antibody was purchased from Abcam (Cambridge, UK).

    Techniques: Expressing, ChIP-sequencing, Binding Assay, Immunoprecipitation, Negative Control, Sequencing