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Elabscience Biotechnology human type i procollagen elisa kit
Scheme of the fabrication of the microcarriers and delivery of engineered nanovesicles for photoaging therapy. Abbreviations: HDF, human dermal fibroblast; Exos, exosomes; Emvs, engineered nanovesicles; HDF COL1A1 Emvs, Emvs derived from HDFs transfected with COL1A1 plasmid (COL1A1 mRNA–encapsulating nanovesicles); ROS, reactive oxygen species; COL1A1, collagen <t>type</t> <t>I</t> alpha 1 chain.
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Advanced Biomatrix Inc vol vol human collagen mixture 3mg ml type i advanced biomatrix 5008
Scheme of the fabrication of the microcarriers and delivery of engineered nanovesicles for photoaging therapy. Abbreviations: HDF, human dermal fibroblast; Exos, exosomes; Emvs, engineered nanovesicles; HDF COL1A1 Emvs, Emvs derived from HDFs transfected with COL1A1 plasmid (COL1A1 mRNA–encapsulating nanovesicles); ROS, reactive oxygen species; COL1A1, collagen <t>type</t> <t>I</t> alpha 1 chain.
Vol Vol Human Collagen Mixture 3mg Ml Type I Advanced Biomatrix 5008, supplied by Advanced Biomatrix Inc, 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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PBL Assay human type i ifn
Human 293T (A, C) and human A549 (B, D) cells were treated with recombinant universal <t>type</t> <t>I</t> <t>IFN</t> or infected with IAV during 24h. TRIM34 gene expression was evaluated by RT-qPCR (A, B) and by Western blot, using an anti-TRIM34 specific antibody, and an anti-GAPDH specific antibody, used as a loading control (C, D) , and compared to the levels in mock-treated or mock-infected cells. Data in A and B represents means and SDs of results from triplicate wells. Three different experiments were performed, with similar results. **p < 0.01 , ***p < 0.001 , ****p < 0.0001; one-way ANOVA followed by Dunnett’s post-hoc test. Protein bands in C and D were quantified using the ImageJ software and normalized to the levels of GAPDH expression (numbers below the blots). TRIM34 positively affects IAV replication in vitro. (E) Human 293T cells were transfected with the pCAGGS plasmid expressing TRIM34-FLAG protein or a pCAGGS empty plasmid, as control. At 24h post-transfection (hpt), cells were mock-infected or infected with IAV (MOI 1). (F) Human 293T cells were transfected twice with a non-targeted (NT) control siRNA or TRIM34 siRNA at two consecutive days, 24 h apart. On day 3, cells were mock-infected or infected with IAV (MOI 1). (E, F) At 0-, 24-, and 48-hours post-infection (hpi), cell culture supernatants were collected and titrated by immunofocus assay in MDCK cells. Data represents means and SDs of results from triplicate wells. Three different experiments were performed, with similar results. *p < 0.05; Student’s t-test with Holm-Šídák correction .
Human Type I Ifn, supplied by PBL Assay, 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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PBL Assay universal type i ifn alpha 11100 1
<t>Type</t> <t>I</t> IFN-induced responses evaluated by RNA sequencing in peripheral blood cells of healthy donors. ( A ) PC analysis was performed using the 500 most variable genes. The percentage of variance retained by the two first components is represented. The donor effect was removed (using the function ‘removeBatchEffect’) from the R package limma, before plotting, and the gene expression levels were normalized using the variance-stabilizing transformation. Samples are colored by the time after exposure to IFN-α. Time is represented in hours. ( B ) Heatmap of the top DEGs (log 2 fold change > 1 and adjusted p value < 0.01 compared with baseline) grouped using hierarchical clustering. The gene expression values were scaled using a Z-score normalization (for each condition, the gene expression value was subtracted from the gene average value and divided by its SD [x – mean/SD]). ( C ) Total number of DEGs (log 2 fold change > 1 and adjusted p value < 0.05) induced by IFN-α at each time point. ( D ) Volcano plot of DEGs affected by IFN-α + placebo at 9 h vs. placebo at baseline. Each gene was plotted as log 2 fold change (x-axis) and −log 10 (adjusted p value [FDR]) (y-axis). The horizontal dashed line indicates the cutoff of −log 10 (adjusted p value) of > 1.3 (adjusted p value < 0.05), and the vertical dashed lines indicate log 2 fold change > 1. ( E ) Gene set enrichment analysis following differential gene expression analysis of peripheral blood cells exposed to placebo + IFN-α at 9 h vs. placebo at 0 h. Hallmark gene sets upregulated (red) and downregulated (blue) are shown. Only significantly modified pathways (adjusted p value < 0.05) are shown as bar plots with the normalized enrichment score on the x-axis. Abbreviations: DEG, differentially expressed gene; FDR, false discovery rate; IFN, interferon; IL, interleukin; JAK, Janus kinase; PC, principal component; SD, standard deviation; STAT, signal transducer and activator of transcription; TNF-α, tumor necrosis factor-α
Universal Type I Ifn Alpha 11100 1, supplied by PBL Assay, 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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MedChemExpress human collagen i
LRRC15 promotes M2 polarization by modulating the ECM production. A, Bar plot showing the enriched pathways of the upregulated genes in TGFβ-treated human CAFs compared with those of LRRC15 -KO CAFs, based on bulk RNA-seq data. B, Scatter plot showing the correlation between the ECM organization signature score and LRRC15 expression level in lung cancer from TCGA. Pearson correlation coefficient R is indicated. C, Bar plot showing the enriched pathways in human LRRC15 + CAFs from lung cancer, based on scRNA-seq data. D, Bar plot showing the enriched pathways in mouse LRRC15 + CAFs from TC1-GFP tumor co-injected with TGFβ-treated CAFs, based on scRNA-seq data. E and F, Collagen expression detected using Sirius Red staining in TGFβ-treated mouse ( E ) and human ( F ) WT or LRRC15 -KO CAFs ( n = 3 wells per group). G, Western blot plots showing <t>collagen</t> <t>I</t> expression in WT or LRRC15 -KO human CAFs treated with or without TGFβ for 48 hours. H, Sirius Red staining of tumors from Col1a2- CreER; Lrrc15 fl/fl and littermate Lrrc15 fl/fl mice bearing KPS tumors ( n = 3–4 mice per group). I, Cell number and proportion of CD206 + BMDMs in mouse BMDM and CAF ECM coculture assay ( n = 3 wells per group). J, Cell number and proportion of CD206 + mo-MΦs in human mo-MΦs and CAF ECM coculture assay ( n = 3 wells per group). K, Proportion and cell number of CD206 + mo-MΦs of CD206 in human mo-MΦs cultured with or without recombinant human collagen I ( n = 3 wells per group). Data are presented as mean ± SEM, Statistical significance was determined using the hypergeometric test ( A , C , and D ) or unpaired two-tailed Student t test ( E , F , H , I , J , and K ). P values were adjusted using the Benjamini–Hochberg method ( A , C , and D ).
Human Collagen I, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bio-Rad anti human type i collagen
LRRC15 promotes M2 polarization by modulating the ECM production. A, Bar plot showing the enriched pathways of the upregulated genes in TGFβ-treated human CAFs compared with those of LRRC15 -KO CAFs, based on bulk RNA-seq data. B, Scatter plot showing the correlation between the ECM organization signature score and LRRC15 expression level in lung cancer from TCGA. Pearson correlation coefficient R is indicated. C, Bar plot showing the enriched pathways in human LRRC15 + CAFs from lung cancer, based on scRNA-seq data. D, Bar plot showing the enriched pathways in mouse LRRC15 + CAFs from TC1-GFP tumor co-injected with TGFβ-treated CAFs, based on scRNA-seq data. E and F, Collagen expression detected using Sirius Red staining in TGFβ-treated mouse ( E ) and human ( F ) WT or LRRC15 -KO CAFs ( n = 3 wells per group). G, Western blot plots showing <t>collagen</t> <t>I</t> expression in WT or LRRC15 -KO human CAFs treated with or without TGFβ for 48 hours. H, Sirius Red staining of tumors from Col1a2- CreER; Lrrc15 fl/fl and littermate Lrrc15 fl/fl mice bearing KPS tumors ( n = 3–4 mice per group). I, Cell number and proportion of CD206 + BMDMs in mouse BMDM and CAF ECM coculture assay ( n = 3 wells per group). J, Cell number and proportion of CD206 + mo-MΦs in human mo-MΦs and CAF ECM coculture assay ( n = 3 wells per group). K, Proportion and cell number of CD206 + mo-MΦs of CD206 in human mo-MΦs cultured with or without recombinant human collagen I ( n = 3 wells per group). Data are presented as mean ± SEM, Statistical significance was determined using the hypergeometric test ( A , C , and D ) or unpaired two-tailed Student t test ( E , F , H , I , J , and K ). P values were adjusted using the Benjamini–Hochberg method ( A , C , and D ).
Anti Human Type I Collagen, supplied by Bio-Rad, 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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R&D Systems recombinant human interferon rhifn proteins
LRRC15 promotes M2 polarization by modulating the ECM production. A, Bar plot showing the enriched pathways of the upregulated genes in TGFβ-treated human CAFs compared with those of LRRC15 -KO CAFs, based on bulk RNA-seq data. B, Scatter plot showing the correlation between the ECM organization signature score and LRRC15 expression level in lung cancer from TCGA. Pearson correlation coefficient R is indicated. C, Bar plot showing the enriched pathways in human LRRC15 + CAFs from lung cancer, based on scRNA-seq data. D, Bar plot showing the enriched pathways in mouse LRRC15 + CAFs from TC1-GFP tumor co-injected with TGFβ-treated CAFs, based on scRNA-seq data. E and F, Collagen expression detected using Sirius Red staining in TGFβ-treated mouse ( E ) and human ( F ) WT or LRRC15 -KO CAFs ( n = 3 wells per group). G, Western blot plots showing <t>collagen</t> <t>I</t> expression in WT or LRRC15 -KO human CAFs treated with or without TGFβ for 48 hours. H, Sirius Red staining of tumors from Col1a2- CreER; Lrrc15 fl/fl and littermate Lrrc15 fl/fl mice bearing KPS tumors ( n = 3–4 mice per group). I, Cell number and proportion of CD206 + BMDMs in mouse BMDM and CAF ECM coculture assay ( n = 3 wells per group). J, Cell number and proportion of CD206 + mo-MΦs in human mo-MΦs and CAF ECM coculture assay ( n = 3 wells per group). K, Proportion and cell number of CD206 + mo-MΦs of CD206 in human mo-MΦs cultured with or without recombinant human collagen I ( n = 3 wells per group). Data are presented as mean ± SEM, Statistical significance was determined using the hypergeometric test ( A , C , and D ) or unpaired two-tailed Student t test ( E , F , H , I , J , and K ). P values were adjusted using the Benjamini–Hochberg method ( A , C , and D ).
Recombinant Human Interferon Rhifn Proteins, supplied by R&D Systems, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+type+i/Recombinant+Human+Universal+Type+I+IFN+Protein%2C+CF/pm41904401-182-0-6
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Proteintech human collagen i
LRRC15 promotes M2 polarization by modulating the ECM production. A, Bar plot showing the enriched pathways of the upregulated genes in TGFβ-treated human CAFs compared with those of LRRC15 -KO CAFs, based on bulk RNA-seq data. B, Scatter plot showing the correlation between the ECM organization signature score and LRRC15 expression level in lung cancer from TCGA. Pearson correlation coefficient R is indicated. C, Bar plot showing the enriched pathways in human LRRC15 + CAFs from lung cancer, based on scRNA-seq data. D, Bar plot showing the enriched pathways in mouse LRRC15 + CAFs from TC1-GFP tumor co-injected with TGFβ-treated CAFs, based on scRNA-seq data. E and F, Collagen expression detected using Sirius Red staining in TGFβ-treated mouse ( E ) and human ( F ) WT or LRRC15 -KO CAFs ( n = 3 wells per group). G, Western blot plots showing <t>collagen</t> <t>I</t> expression in WT or LRRC15 -KO human CAFs treated with or without TGFβ for 48 hours. H, Sirius Red staining of tumors from Col1a2- CreER; Lrrc15 fl/fl and littermate Lrrc15 fl/fl mice bearing KPS tumors ( n = 3–4 mice per group). I, Cell number and proportion of CD206 + BMDMs in mouse BMDM and CAF ECM coculture assay ( n = 3 wells per group). J, Cell number and proportion of CD206 + mo-MΦs in human mo-MΦs and CAF ECM coculture assay ( n = 3 wells per group). K, Proportion and cell number of CD206 + mo-MΦs of CD206 in human mo-MΦs cultured with or without recombinant human collagen I ( n = 3 wells per group). Data are presented as mean ± SEM, Statistical significance was determined using the hypergeometric test ( A , C , and D ) or unpaired two-tailed Student t test ( E , F , H , I , J , and K ). P values were adjusted using the Benjamini–Hochberg method ( A , C , and D ).
Human Collagen I, 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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Image Search Results


Scheme of the fabrication of the microcarriers and delivery of engineered nanovesicles for photoaging therapy. Abbreviations: HDF, human dermal fibroblast; Exos, exosomes; Emvs, engineered nanovesicles; HDF COL1A1 Emvs, Emvs derived from HDFs transfected with COL1A1 plasmid (COL1A1 mRNA–encapsulating nanovesicles); ROS, reactive oxygen species; COL1A1, collagen type I alpha 1 chain.

Journal: Materials Today Bio

Article Title: Microcarriers encapsulating COL1A1 mRNA-loaded nanovesicles for skin photoaging treatment

doi: 10.1016/j.mtbio.2026.103126

Figure Lengend Snippet: Scheme of the fabrication of the microcarriers and delivery of engineered nanovesicles for photoaging therapy. Abbreviations: HDF, human dermal fibroblast; Exos, exosomes; Emvs, engineered nanovesicles; HDF COL1A1 Emvs, Emvs derived from HDFs transfected with COL1A1 plasmid (COL1A1 mRNA–encapsulating nanovesicles); ROS, reactive oxygen species; COL1A1, collagen type I alpha 1 chain.

Article Snippet: The concentration of human type I procollagen was measured using a human type I procollagen ELISA kit (Elabscience Biotechnology, China) according to the manufacturer's instructions.

Techniques: Derivative Assay, Transfection, Plasmid Preparation

In vivo biosafety evaluation. a) In vivo imaging of subcutaneous injection sites across different groups. b) Quantification of relative fluorescence intensity (n = 5). c) Histological analysis via H&E staining of the heart, liver, spleen, lung, and kidney tissues. d) ELISA quantification of IL-6 levels and TNF-α levels (n = 5). e) Quantification of ALT, AST, CREA, and UA levels (n = 3). The scale bar is 300 μm in c).

Journal: Materials Today Bio

Article Title: Microcarriers encapsulating COL1A1 mRNA-loaded nanovesicles for skin photoaging treatment

doi: 10.1016/j.mtbio.2026.103126

Figure Lengend Snippet: In vivo biosafety evaluation. a) In vivo imaging of subcutaneous injection sites across different groups. b) Quantification of relative fluorescence intensity (n = 5). c) Histological analysis via H&E staining of the heart, liver, spleen, lung, and kidney tissues. d) ELISA quantification of IL-6 levels and TNF-α levels (n = 5). e) Quantification of ALT, AST, CREA, and UA levels (n = 3). The scale bar is 300 μm in c).

Article Snippet: The concentration of human type I procollagen was measured using a human type I procollagen ELISA kit (Elabscience Biotechnology, China) according to the manufacturer's instructions.

Techniques: In Vivo, In Vivo Imaging, Injection, Fluorescence, Staining, Enzyme-linked Immunosorbent Assay

Human 293T (A, C) and human A549 (B, D) cells were treated with recombinant universal type I IFN or infected with IAV during 24h. TRIM34 gene expression was evaluated by RT-qPCR (A, B) and by Western blot, using an anti-TRIM34 specific antibody, and an anti-GAPDH specific antibody, used as a loading control (C, D) , and compared to the levels in mock-treated or mock-infected cells. Data in A and B represents means and SDs of results from triplicate wells. Three different experiments were performed, with similar results. **p < 0.01 , ***p < 0.001 , ****p < 0.0001; one-way ANOVA followed by Dunnett’s post-hoc test. Protein bands in C and D were quantified using the ImageJ software and normalized to the levels of GAPDH expression (numbers below the blots). TRIM34 positively affects IAV replication in vitro. (E) Human 293T cells were transfected with the pCAGGS plasmid expressing TRIM34-FLAG protein or a pCAGGS empty plasmid, as control. At 24h post-transfection (hpt), cells were mock-infected or infected with IAV (MOI 1). (F) Human 293T cells were transfected twice with a non-targeted (NT) control siRNA or TRIM34 siRNA at two consecutive days, 24 h apart. On day 3, cells were mock-infected or infected with IAV (MOI 1). (E, F) At 0-, 24-, and 48-hours post-infection (hpi), cell culture supernatants were collected and titrated by immunofocus assay in MDCK cells. Data represents means and SDs of results from triplicate wells. Three different experiments were performed, with similar results. *p < 0.05; Student’s t-test with Holm-Šídák correction .

Journal: PLOS Pathogens

Article Title: Tripartite motif-containing 34 (TRIM34) protein interacts with the nucleocytoplasmic transport machinery and negatively modulates antiviral responses

doi: 10.1371/journal.ppat.1014142

Figure Lengend Snippet: Human 293T (A, C) and human A549 (B, D) cells were treated with recombinant universal type I IFN or infected with IAV during 24h. TRIM34 gene expression was evaluated by RT-qPCR (A, B) and by Western blot, using an anti-TRIM34 specific antibody, and an anti-GAPDH specific antibody, used as a loading control (C, D) , and compared to the levels in mock-treated or mock-infected cells. Data in A and B represents means and SDs of results from triplicate wells. Three different experiments were performed, with similar results. **p < 0.01 , ***p < 0.001 , ****p < 0.0001; one-way ANOVA followed by Dunnett’s post-hoc test. Protein bands in C and D were quantified using the ImageJ software and normalized to the levels of GAPDH expression (numbers below the blots). TRIM34 positively affects IAV replication in vitro. (E) Human 293T cells were transfected with the pCAGGS plasmid expressing TRIM34-FLAG protein or a pCAGGS empty plasmid, as control. At 24h post-transfection (hpt), cells were mock-infected or infected with IAV (MOI 1). (F) Human 293T cells were transfected twice with a non-targeted (NT) control siRNA or TRIM34 siRNA at two consecutive days, 24 h apart. On day 3, cells were mock-infected or infected with IAV (MOI 1). (E, F) At 0-, 24-, and 48-hours post-infection (hpi), cell culture supernatants were collected and titrated by immunofocus assay in MDCK cells. Data represents means and SDs of results from triplicate wells. Three different experiments were performed, with similar results. *p < 0.05; Student’s t-test with Holm-Šídák correction .

Article Snippet: Furthermore, human 293T, A549 or BEAS-2B cells were treated with different concentrations of recombinant human type I IFN (11200–2, PBL Assay Science) during 24h.

Techniques: Recombinant, Infection, Gene Expression, Quantitative RT-PCR, Western Blot, Control, Software, Expressing, In Vitro, Transfection, Plasmid Preparation, Cell Culture

(A, B) Human 293T cells were transfected with the plasmid pCAGGs-TRIM34-FLAG or the empty control plasmid. (A) At 24h post-transfection, cells were non-treated or treated with type I IFN. At 24h post-IFN-treatment, CXCL10, IFNB1, IFNL1 and IFIT2 expression was measured by RT-qPCR and mRNA levels were expressed as fold-change (increases) in comparison to mock-treated cells transfected with the empty plasmid, used as control. (B) At 24h post-IFN-treatment, cells were infected with rVSV-GFP (MOI 0.1) and viral titers were measured by lysis plaque assay at 24hpi. Data represents means and SDs of results from triplicate wells. Three different experiments were performed, with similar results. *p < 0.05 for comparisons between empty and TRIM34 overexpressed cells using Student’s t-test with Holm-Šídák correction . Human 293T cells (C, F) , human lung adenocarcinoma-derived cells A549 cells (D, G), or the non-tumorigenic human bronchial epithelial BEAS-2B (E, H) were transfected twice with NT control siRNA or TRIM34 siRNA, 24h apart, for two consecutive days. On day 3, cells were treated with IFN for an additional 24h. (C, D, E) TRIM34, and (F, G, H) CXCL10, IFNB1, IFNL1 and IFIT2 expression was measured by RT-qPCR and mRNA levels were expressed as fold-change (increases) in comparison to mock-treated cells, transfected with the NT siRNA, used as control. (A-H) Data represents means and SDs of results from triplicate wells. Three different experiments were performed, with similar results. *p < 0.05 for comparisons between control and TRIM34 knocked-down cells using Student’s t-test with Holm-Šídák correction .

Journal: PLOS Pathogens

Article Title: Tripartite motif-containing 34 (TRIM34) protein interacts with the nucleocytoplasmic transport machinery and negatively modulates antiviral responses

doi: 10.1371/journal.ppat.1014142

Figure Lengend Snippet: (A, B) Human 293T cells were transfected with the plasmid pCAGGs-TRIM34-FLAG or the empty control plasmid. (A) At 24h post-transfection, cells were non-treated or treated with type I IFN. At 24h post-IFN-treatment, CXCL10, IFNB1, IFNL1 and IFIT2 expression was measured by RT-qPCR and mRNA levels were expressed as fold-change (increases) in comparison to mock-treated cells transfected with the empty plasmid, used as control. (B) At 24h post-IFN-treatment, cells were infected with rVSV-GFP (MOI 0.1) and viral titers were measured by lysis plaque assay at 24hpi. Data represents means and SDs of results from triplicate wells. Three different experiments were performed, with similar results. *p < 0.05 for comparisons between empty and TRIM34 overexpressed cells using Student’s t-test with Holm-Šídák correction . Human 293T cells (C, F) , human lung adenocarcinoma-derived cells A549 cells (D, G), or the non-tumorigenic human bronchial epithelial BEAS-2B (E, H) were transfected twice with NT control siRNA or TRIM34 siRNA, 24h apart, for two consecutive days. On day 3, cells were treated with IFN for an additional 24h. (C, D, E) TRIM34, and (F, G, H) CXCL10, IFNB1, IFNL1 and IFIT2 expression was measured by RT-qPCR and mRNA levels were expressed as fold-change (increases) in comparison to mock-treated cells, transfected with the NT siRNA, used as control. (A-H) Data represents means and SDs of results from triplicate wells. Three different experiments were performed, with similar results. *p < 0.05 for comparisons between control and TRIM34 knocked-down cells using Student’s t-test with Holm-Šídák correction .

Article Snippet: Furthermore, human 293T, A549 or BEAS-2B cells were treated with different concentrations of recombinant human type I IFN (11200–2, PBL Assay Science) during 24h.

Techniques: Transfection, Plasmid Preparation, Control, Expressing, Quantitative RT-PCR, Comparison, Infection, Lysis, Plaque Assay, Derivative Assay

Type I IFN-induced responses evaluated by RNA sequencing in peripheral blood cells of healthy donors. ( A ) PC analysis was performed using the 500 most variable genes. The percentage of variance retained by the two first components is represented. The donor effect was removed (using the function ‘removeBatchEffect’) from the R package limma, before plotting, and the gene expression levels were normalized using the variance-stabilizing transformation. Samples are colored by the time after exposure to IFN-α. Time is represented in hours. ( B ) Heatmap of the top DEGs (log 2 fold change > 1 and adjusted p value < 0.01 compared with baseline) grouped using hierarchical clustering. The gene expression values were scaled using a Z-score normalization (for each condition, the gene expression value was subtracted from the gene average value and divided by its SD [x – mean/SD]). ( C ) Total number of DEGs (log 2 fold change > 1 and adjusted p value < 0.05) induced by IFN-α at each time point. ( D ) Volcano plot of DEGs affected by IFN-α + placebo at 9 h vs. placebo at baseline. Each gene was plotted as log 2 fold change (x-axis) and −log 10 (adjusted p value [FDR]) (y-axis). The horizontal dashed line indicates the cutoff of −log 10 (adjusted p value) of > 1.3 (adjusted p value < 0.05), and the vertical dashed lines indicate log 2 fold change > 1. ( E ) Gene set enrichment analysis following differential gene expression analysis of peripheral blood cells exposed to placebo + IFN-α at 9 h vs. placebo at 0 h. Hallmark gene sets upregulated (red) and downregulated (blue) are shown. Only significantly modified pathways (adjusted p value < 0.05) are shown as bar plots with the normalized enrichment score on the x-axis. Abbreviations: DEG, differentially expressed gene; FDR, false discovery rate; IFN, interferon; IL, interleukin; JAK, Janus kinase; PC, principal component; SD, standard deviation; STAT, signal transducer and activator of transcription; TNF-α, tumor necrosis factor-α

Journal: Inflammation

Article Title: Pharmacological Characterization of GLPG3667, a Tyrosine Kinase 2-Selective Inhibitor, for the Treatment of Inflammatory and Autoimmune Diseases

doi: 10.1007/s10753-026-02519-1

Figure Lengend Snippet: Type I IFN-induced responses evaluated by RNA sequencing in peripheral blood cells of healthy donors. ( A ) PC analysis was performed using the 500 most variable genes. The percentage of variance retained by the two first components is represented. The donor effect was removed (using the function ‘removeBatchEffect’) from the R package limma, before plotting, and the gene expression levels were normalized using the variance-stabilizing transformation. Samples are colored by the time after exposure to IFN-α. Time is represented in hours. ( B ) Heatmap of the top DEGs (log 2 fold change > 1 and adjusted p value < 0.01 compared with baseline) grouped using hierarchical clustering. The gene expression values were scaled using a Z-score normalization (for each condition, the gene expression value was subtracted from the gene average value and divided by its SD [x – mean/SD]). ( C ) Total number of DEGs (log 2 fold change > 1 and adjusted p value < 0.05) induced by IFN-α at each time point. ( D ) Volcano plot of DEGs affected by IFN-α + placebo at 9 h vs. placebo at baseline. Each gene was plotted as log 2 fold change (x-axis) and −log 10 (adjusted p value [FDR]) (y-axis). The horizontal dashed line indicates the cutoff of −log 10 (adjusted p value) of > 1.3 (adjusted p value < 0.05), and the vertical dashed lines indicate log 2 fold change > 1. ( E ) Gene set enrichment analysis following differential gene expression analysis of peripheral blood cells exposed to placebo + IFN-α at 9 h vs. placebo at 0 h. Hallmark gene sets upregulated (red) and downregulated (blue) are shown. Only significantly modified pathways (adjusted p value < 0.05) are shown as bar plots with the normalized enrichment score on the x-axis. Abbreviations: DEG, differentially expressed gene; FDR, false discovery rate; IFN, interferon; IL, interleukin; JAK, Janus kinase; PC, principal component; SD, standard deviation; STAT, signal transducer and activator of transcription; TNF-α, tumor necrosis factor-α

Article Snippet: After the incubation period, release of IFN-γ-induced protein 10 (IP-10) was triggered with 3000 U/mL IFN-α (Universal Type I IFN-Alpha, 11100-1, PBL Assay Science, PBL) for 24 h at 37 °C.

Techniques: RNA Sequencing, Gene Expression, Transformation Assay, Modification, Standard Deviation

LRRC15 promotes M2 polarization by modulating the ECM production. A, Bar plot showing the enriched pathways of the upregulated genes in TGFβ-treated human CAFs compared with those of LRRC15 -KO CAFs, based on bulk RNA-seq data. B, Scatter plot showing the correlation between the ECM organization signature score and LRRC15 expression level in lung cancer from TCGA. Pearson correlation coefficient R is indicated. C, Bar plot showing the enriched pathways in human LRRC15 + CAFs from lung cancer, based on scRNA-seq data. D, Bar plot showing the enriched pathways in mouse LRRC15 + CAFs from TC1-GFP tumor co-injected with TGFβ-treated CAFs, based on scRNA-seq data. E and F, Collagen expression detected using Sirius Red staining in TGFβ-treated mouse ( E ) and human ( F ) WT or LRRC15 -KO CAFs ( n = 3 wells per group). G, Western blot plots showing collagen I expression in WT or LRRC15 -KO human CAFs treated with or without TGFβ for 48 hours. H, Sirius Red staining of tumors from Col1a2- CreER; Lrrc15 fl/fl and littermate Lrrc15 fl/fl mice bearing KPS tumors ( n = 3–4 mice per group). I, Cell number and proportion of CD206 + BMDMs in mouse BMDM and CAF ECM coculture assay ( n = 3 wells per group). J, Cell number and proportion of CD206 + mo-MΦs in human mo-MΦs and CAF ECM coculture assay ( n = 3 wells per group). K, Proportion and cell number of CD206 + mo-MΦs of CD206 in human mo-MΦs cultured with or without recombinant human collagen I ( n = 3 wells per group). Data are presented as mean ± SEM, Statistical significance was determined using the hypergeometric test ( A , C , and D ) or unpaired two-tailed Student t test ( E , F , H , I , J , and K ). P values were adjusted using the Benjamini–Hochberg method ( A , C , and D ).

Journal: Cancer Research

Article Title: Targeting LRRC15 in Cancer-Associated Fibroblasts Modifies the Extracellular Matrix and Enhances Tumor Immune Responses to Suppress Lung Cancer Progression

doi: 10.1158/0008-5472.CAN-25-2871

Figure Lengend Snippet: LRRC15 promotes M2 polarization by modulating the ECM production. A, Bar plot showing the enriched pathways of the upregulated genes in TGFβ-treated human CAFs compared with those of LRRC15 -KO CAFs, based on bulk RNA-seq data. B, Scatter plot showing the correlation between the ECM organization signature score and LRRC15 expression level in lung cancer from TCGA. Pearson correlation coefficient R is indicated. C, Bar plot showing the enriched pathways in human LRRC15 + CAFs from lung cancer, based on scRNA-seq data. D, Bar plot showing the enriched pathways in mouse LRRC15 + CAFs from TC1-GFP tumor co-injected with TGFβ-treated CAFs, based on scRNA-seq data. E and F, Collagen expression detected using Sirius Red staining in TGFβ-treated mouse ( E ) and human ( F ) WT or LRRC15 -KO CAFs ( n = 3 wells per group). G, Western blot plots showing collagen I expression in WT or LRRC15 -KO human CAFs treated with or without TGFβ for 48 hours. H, Sirius Red staining of tumors from Col1a2- CreER; Lrrc15 fl/fl and littermate Lrrc15 fl/fl mice bearing KPS tumors ( n = 3–4 mice per group). I, Cell number and proportion of CD206 + BMDMs in mouse BMDM and CAF ECM coculture assay ( n = 3 wells per group). J, Cell number and proportion of CD206 + mo-MΦs in human mo-MΦs and CAF ECM coculture assay ( n = 3 wells per group). K, Proportion and cell number of CD206 + mo-MΦs of CD206 in human mo-MΦs cultured with or without recombinant human collagen I ( n = 3 wells per group). Data are presented as mean ± SEM, Statistical significance was determined using the hypergeometric test ( A , C , and D ) or unpaired two-tailed Student t test ( E , F , H , I , J , and K ). P values were adjusted using the Benjamini–Hochberg method ( A , C , and D ).

Article Snippet: For macrophage–collagen stimulation assays, 500 μg/mL human collagen I (MedChemExpress, cat. #HY-NP160) was coated in 12-well plates for culturing mo-MΦs.

Techniques: RNA Sequencing, Expressing, Injection, Staining, Western Blot, Co-culture Assay, Cell Culture, Recombinant, Two Tailed Test