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MedChemExpress cyclin d1 mediated mce
Cyclin D1 Mediated Mce, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech mouse monoclonal anti human cyclin d1
Downstream signaling pathway of BTG1 in AML cell lines (A) Top three signaling pathways in terms of Gene Ratio were EBV infection (0.037), Wnt signaling pathway (0.035), and hematopoietic lineage (0.023) of KEGG pathway enrichment. (B) Effect of BTG1 on the mRNA expression of β-catenin, <t>Cyclin</t> <t>D1,</t> and C-Myc. (C) Effect of BTG1 on the protein expression of β-catenin and Cyclin D1. (D) The relative viability of AML cells after interference of BTG1 and treatment with FH535. (E) Apoptosis of AML cells after interference of BTG1 and treatment with FH535. Data are presented as mean ± standard deviation (SD). (ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001).
Mouse Monoclonal Anti Human Cyclin D1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech mouse anti human ccnd1 antibody
a. Heatmap depicting the top 20 differentially expressed genes between STAG2 wildtype and mutant populations. b. Using gene set enrichment analysis (GSEA), only the “HALLMARK_TNFA_SIGNALING_VIA_NFKB” gene set was upregulated in wildtype compared to mutant (Normalised enrichment score: 1.75, False discovery rate q -value: 0.078). c. On immunofluorescence staining, we observed increased proliferation of wildtype organoids relative to STAG2 mutants when stained with anti-KI67 antibody. d. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. e. We also observed increased tumorigenicity of wildtype organoids relative to STAG2 mutants when stained with <t>anti-CCND1</t> antibody. f. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. Scale bars are 50µm. All experiments were performed with N = 3 biological replicates.
Mouse Anti Human Ccnd1 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse anti human ccnd1 antibody - by Bioz Stars, 2026-03
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MedChemExpress cyclin d1
a. Heatmap depicting the top 20 differentially expressed genes between STAG2 wildtype and mutant populations. b. Using gene set enrichment analysis (GSEA), only the “HALLMARK_TNFA_SIGNALING_VIA_NFKB” gene set was upregulated in wildtype compared to mutant (Normalised enrichment score: 1.75, False discovery rate q -value: 0.078). c. On immunofluorescence staining, we observed increased proliferation of wildtype organoids relative to STAG2 mutants when stained with anti-KI67 antibody. d. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. e. We also observed increased tumorigenicity of wildtype organoids relative to STAG2 mutants when stained with <t>anti-CCND1</t> antibody. f. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. Scale bars are 50µm. All experiments were performed with N = 3 biological replicates.
Cyclin D1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress mce ↓ cyclin d1 ↓ cyclin
Predicted differences in microRNA (miR)-mediated adipogenic gene regulation between formula feeding and breastfeeding. ( A ) Formula feeding with increased protein intake and deficient miR supply increases the expression of FTO . FTO-mediated m 6 A demethylation enhances gene expression of activators of cell cycle progression ( MYC , <t>CCND1</t> ), adipogenic transcription factors ( PPARG , CEBPA , CEBPB ), ATF4 (increasing leucine (Leu)-mediated mTORC1/S6K1 activation), upregulation of FLOT2 (promoting adipogenic extracellular matrix (ECM) changes), upregulation of PDGFRB (increasing adipocyte precursor cell (APC) retention in the vascular niche as well as enhanced VEGFA expression (increasing angiogenesis and APC niche expansion) synergistically promoting adipocyte stem cell (ASC) mitotic clonal expansion (MCE), wingless (WNT) suppression-regulated ASC commitment and adipogenesis. ( B ) Early lactation-derived breast milk exosomal miRs attenuate FTO expression resulting in reduced expression of FTO-activated adipogenic transcription factors and regulators of ASC development (green color) in the vascular niche and ECM. Increased Wnt signaling attenuates ASC commitment and APC expansion adjusting ASC numbers and differentiation. Complete names of gene symbols are provided in the list of abbreviations. FTO-regulated genes are presented in green color.
Mce ↓ Cyclin D1 ↓ Cyclin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress kinases cyclin d1 cdk4
Predicted differences in microRNA (miR)-mediated adipogenic gene regulation between formula feeding and breastfeeding. ( A ) Formula feeding with increased protein intake and deficient miR supply increases the expression of FTO . FTO-mediated m 6 A demethylation enhances gene expression of activators of cell cycle progression ( MYC , <t>CCND1</t> ), adipogenic transcription factors ( PPARG , CEBPA , CEBPB ), ATF4 (increasing leucine (Leu)-mediated mTORC1/S6K1 activation), upregulation of FLOT2 (promoting adipogenic extracellular matrix (ECM) changes), upregulation of PDGFRB (increasing adipocyte precursor cell (APC) retention in the vascular niche as well as enhanced VEGFA expression (increasing angiogenesis and APC niche expansion) synergistically promoting adipocyte stem cell (ASC) mitotic clonal expansion (MCE), wingless (WNT) suppression-regulated ASC commitment and adipogenesis. ( B ) Early lactation-derived breast milk exosomal miRs attenuate FTO expression resulting in reduced expression of FTO-activated adipogenic transcription factors and regulators of ASC development (green color) in the vascular niche and ECM. Increased Wnt signaling attenuates ASC commitment and APC expansion adjusting ASC numbers and differentiation. Complete names of gene symbols are provided in the list of abbreviations. FTO-regulated genes are presented in green color.
Kinases Cyclin D1 Cdk4, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress cyclin d1 cdk6
Predicted differences in microRNA (miR)-mediated adipogenic gene regulation between formula feeding and breastfeeding. ( A ) Formula feeding with increased protein intake and deficient miR supply increases the expression of FTO . FTO-mediated m 6 A demethylation enhances gene expression of activators of cell cycle progression ( MYC , <t>CCND1</t> ), adipogenic transcription factors ( PPARG , CEBPA , CEBPB ), ATF4 (increasing leucine (Leu)-mediated mTORC1/S6K1 activation), upregulation of FLOT2 (promoting adipogenic extracellular matrix (ECM) changes), upregulation of PDGFRB (increasing adipocyte precursor cell (APC) retention in the vascular niche as well as enhanced VEGFA expression (increasing angiogenesis and APC niche expansion) synergistically promoting adipocyte stem cell (ASC) mitotic clonal expansion (MCE), wingless (WNT) suppression-regulated ASC commitment and adipogenesis. ( B ) Early lactation-derived breast milk exosomal miRs attenuate FTO expression resulting in reduced expression of FTO-activated adipogenic transcription factors and regulators of ASC development (green color) in the vascular niche and ECM. Increased Wnt signaling attenuates ASC commitment and APC expansion adjusting ASC numbers and differentiation. Complete names of gene symbols are provided in the list of abbreviations. FTO-regulated genes are presented in green color.
Cyclin D1 Cdk6, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Downstream signaling pathway of BTG1 in AML cell lines (A) Top three signaling pathways in terms of Gene Ratio were EBV infection (0.037), Wnt signaling pathway (0.035), and hematopoietic lineage (0.023) of KEGG pathway enrichment. (B) Effect of BTG1 on the mRNA expression of β-catenin, Cyclin D1, and C-Myc. (C) Effect of BTG1 on the protein expression of β-catenin and Cyclin D1. (D) The relative viability of AML cells after interference of BTG1 and treatment with FH535. (E) Apoptosis of AML cells after interference of BTG1 and treatment with FH535. Data are presented as mean ± standard deviation (SD). (ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001).

Journal: iScience

Article Title: Prognostic value of BTG1 for predicting decitabine sensitivity in de novo acute myeloid leukemia

doi: 10.1016/j.isci.2025.114327

Figure Lengend Snippet: Downstream signaling pathway of BTG1 in AML cell lines (A) Top three signaling pathways in terms of Gene Ratio were EBV infection (0.037), Wnt signaling pathway (0.035), and hematopoietic lineage (0.023) of KEGG pathway enrichment. (B) Effect of BTG1 on the mRNA expression of β-catenin, Cyclin D1, and C-Myc. (C) Effect of BTG1 on the protein expression of β-catenin and Cyclin D1. (D) The relative viability of AML cells after interference of BTG1 and treatment with FH535. (E) Apoptosis of AML cells after interference of BTG1 and treatment with FH535. Data are presented as mean ± standard deviation (SD). (ns, p > 0.05; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001).

Article Snippet: Mouse monoclonal anti-human Cyclin D1 , Proteintech , Cat# 60186-1-Ig RRID: AB_10793718.

Techniques: Protein-Protein interactions, Infection, Expressing, Standard Deviation

a. Heatmap depicting the top 20 differentially expressed genes between STAG2 wildtype and mutant populations. b. Using gene set enrichment analysis (GSEA), only the “HALLMARK_TNFA_SIGNALING_VIA_NFKB” gene set was upregulated in wildtype compared to mutant (Normalised enrichment score: 1.75, False discovery rate q -value: 0.078). c. On immunofluorescence staining, we observed increased proliferation of wildtype organoids relative to STAG2 mutants when stained with anti-KI67 antibody. d. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. e. We also observed increased tumorigenicity of wildtype organoids relative to STAG2 mutants when stained with anti-CCND1 antibody. f. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. Scale bars are 50µm. All experiments were performed with N = 3 biological replicates.

Journal: PLOS One

Article Title: STAG2 mutations in the normal colon induce upregulation of oncogenic pathways in neighbouring wildtype cells

doi: 10.1371/journal.pone.0332499

Figure Lengend Snippet: a. Heatmap depicting the top 20 differentially expressed genes between STAG2 wildtype and mutant populations. b. Using gene set enrichment analysis (GSEA), only the “HALLMARK_TNFA_SIGNALING_VIA_NFKB” gene set was upregulated in wildtype compared to mutant (Normalised enrichment score: 1.75, False discovery rate q -value: 0.078). c. On immunofluorescence staining, we observed increased proliferation of wildtype organoids relative to STAG2 mutants when stained with anti-KI67 antibody. d. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. e. We also observed increased tumorigenicity of wildtype organoids relative to STAG2 mutants when stained with anti-CCND1 antibody. f. Fluorescent intensity of anti-KI67 antibody was statistically significantly upregulated in co-cultured wildtype organoids relative to STAG2 mutant organoids. Scale bars are 50µm. All experiments were performed with N = 3 biological replicates.

Article Snippet: Primary antibodies used included rabbit anti-human STAG2 antibody (1:100, 19837–1-AP, Proteintech, USA), mouse anti-human KI67 antibody (1:500, 66555–6-Ig, Proteintech, USA), mouse anti-human P53 antibody (1:400, 60283–2-Ig, Proteintech, USA), mouse anti-human CCND1 antibody (1:100, 60186–1-Ig, Proteintech, USA), mouse anti-human TERT antibody (1: 100, MA5−16033, Invitrogen, USA), mouse anti-human KRAS antibody (1:250, 415700, Invitrogen, USA), and mouse anti-human TNFα antibody (1:50, MA5−23720, Invitrogen, USA).

Techniques: Mutagenesis, Immunofluorescence, Staining, Cell Culture

Predicted differences in microRNA (miR)-mediated adipogenic gene regulation between formula feeding and breastfeeding. ( A ) Formula feeding with increased protein intake and deficient miR supply increases the expression of FTO . FTO-mediated m 6 A demethylation enhances gene expression of activators of cell cycle progression ( MYC , CCND1 ), adipogenic transcription factors ( PPARG , CEBPA , CEBPB ), ATF4 (increasing leucine (Leu)-mediated mTORC1/S6K1 activation), upregulation of FLOT2 (promoting adipogenic extracellular matrix (ECM) changes), upregulation of PDGFRB (increasing adipocyte precursor cell (APC) retention in the vascular niche as well as enhanced VEGFA expression (increasing angiogenesis and APC niche expansion) synergistically promoting adipocyte stem cell (ASC) mitotic clonal expansion (MCE), wingless (WNT) suppression-regulated ASC commitment and adipogenesis. ( B ) Early lactation-derived breast milk exosomal miRs attenuate FTO expression resulting in reduced expression of FTO-activated adipogenic transcription factors and regulators of ASC development (green color) in the vascular niche and ECM. Increased Wnt signaling attenuates ASC commitment and APC expansion adjusting ASC numbers and differentiation. Complete names of gene symbols are provided in the list of abbreviations. FTO-regulated genes are presented in green color.

Journal: International Journal of Molecular Sciences

Article Title: White Adipocyte Stem Cell Expansion Through Infant Formula Feeding: New Insights into Epigenetic Programming Explaining the Early Protein Hypothesis of Obesity

doi: 10.3390/ijms26104493

Figure Lengend Snippet: Predicted differences in microRNA (miR)-mediated adipogenic gene regulation between formula feeding and breastfeeding. ( A ) Formula feeding with increased protein intake and deficient miR supply increases the expression of FTO . FTO-mediated m 6 A demethylation enhances gene expression of activators of cell cycle progression ( MYC , CCND1 ), adipogenic transcription factors ( PPARG , CEBPA , CEBPB ), ATF4 (increasing leucine (Leu)-mediated mTORC1/S6K1 activation), upregulation of FLOT2 (promoting adipogenic extracellular matrix (ECM) changes), upregulation of PDGFRB (increasing adipocyte precursor cell (APC) retention in the vascular niche as well as enhanced VEGFA expression (increasing angiogenesis and APC niche expansion) synergistically promoting adipocyte stem cell (ASC) mitotic clonal expansion (MCE), wingless (WNT) suppression-regulated ASC commitment and adipogenesis. ( B ) Early lactation-derived breast milk exosomal miRs attenuate FTO expression resulting in reduced expression of FTO-activated adipogenic transcription factors and regulators of ASC development (green color) in the vascular niche and ECM. Increased Wnt signaling attenuates ASC commitment and APC expansion adjusting ASC numbers and differentiation. Complete names of gene symbols are provided in the list of abbreviations. FTO-regulated genes are presented in green color.

Article Snippet: MiR-34a-5p , CCND1 CCNE1 CDK2 CDK4 CDK6 PDGFRB CTRP9 FLOT2 , Cyclin D1 ↓ , inhibition of ASC differentiation, MCE ↓ Cyclin D1 ↓ Cyclin-dependent kinase 2 ↓ Cyclin-dependent kinase 4 ↓ Cyclin-dependent kinase 6 Platelet-derived growth factor receptor B ↓ , suppression of ASC niche formation Suppression of ASC proliferation and migration Flotillin 2 ↓ , suppression of pro-adipogenic ECM , [ ] [ , ] [ ] [ , ] .

Techniques: Expressing, Gene Expression, Activation Assay, Derivative Assay