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Image Search Results
Journal: Polymers
Article Title: Comprehensive Analysis of Chromatin Accessibility and Transcriptional Landscape Identified BRCA1 Repression as a Potential Pathological Factor for Keloid
doi: 10.3390/polym14163391
Figure Lengend Snippet: Suppressed BRCA1 expression is a potential pathogenic factor in keloid. ( A ) Protein–protein interaction (PPI) network of DEGs based on STRING database. More lines between two genes indicates more reliable interactions between them, and line color represents evidence type for their interaction. BRCA1 as a hub gene, i.e., highly connected in the network, is highlighted by a red arrow. ( B ) Validation of down-regulation of BRCA1 in keloid DF compared with normal DF, as well as in shBRCA1 and shSCR DF samples by RT-PCR. ( C ) Validation of the suppression of BRCA1 by small hairpin RNA (shRNA) by RT-PCR in normal DF. ( D ) Relative cell viability of normal DF that transfected with shRNA for BRCA1 (shB1) or control (shSCR) quantified by CCK-8 method. ( E ) Wound-healing ability of normal DF that transfected with shB1 or shSCR and quantified by scratch test. The left panel shows the representative DF wound-healing examples and the right panel illustrating the wound closure percent of shB1 and shSCR DF at different time points. Error bars represent the mean ± standard deviation (SD) of three independent experiments. n.s., not significant; * p value < 0.05.
Article Snippet: The following antibodies were used:
Techniques: Expressing, Biomarker Discovery, Reverse Transcription Polymerase Chain Reaction, shRNA, Transfection, Control, CCK-8 Assay, Standard Deviation
Journal: Polymers
Article Title: Comprehensive Analysis of Chromatin Accessibility and Transcriptional Landscape Identified BRCA1 Repression as a Potential Pathological Factor for Keloid
doi: 10.3390/polym14163391
Figure Lengend Snippet: BRCA1 associates with molecular events related to keloid formation in normal DF. ( A ) Volcano plot illustrating the log2-based fold change (X-axis) and significance (Y-axis, log10-based p value) of differential expression analysis between shB1 and shSCR DF samples. Blue and red dots are significantly down- and upregulated genes in normal shB1 DF relative to normal shSCR DF, respectively. Dark grey dots represent non-significantly differential expression genes. ( B ) Heatmap of z-score normalized expression values of DEGs in normal shB1 and shSCR DF. ( C ) and ( D ) represent the significantly enriched GO terms and KEGG pathways of DEGs, respectively. CEMT, cardiac epithelial to mesenchymal transition.
Article Snippet: The following antibodies were used:
Techniques: Quantitative Proteomics, Expressing
Journal: Polymers
Article Title: Comprehensive Analysis of Chromatin Accessibility and Transcriptional Landscape Identified BRCA1 Repression as a Potential Pathological Factor for Keloid
doi: 10.3390/polym14163391
Figure Lengend Snippet: BRCA1 might regulate NPTX2 expression by manipulating its enhancer accessibility and influencing enhancer–promoter interactions in normal DF. ( A ) Heatmap of the log2-based fold change of genes that significantly affected differential expression in both shB1 normal DF compared with shSCR normal DF and keloid DF compared with normal DF. LFC, log2-based fold change. ( B ) Validation of down-regulation of NPTX2 in keloid DF relative to normal DF (upper panel) and shB1 normal DF relative to shSCR normal DF (bottom panel). ( C ) Density profile of H3K27ac and H3K4me1 CUT&Tag-seq in keloid DF, ATAC-seq in normal and keloid DF, BRCA1 CUT&Tag-seq in normal and keloid DF at NPTX2 as well as its associated enhancer region. Interaction between NPTX2 enhancer and promoter predicted based on GeneHancer database is shown in bottom. H, normal DF; K, keloid DF. The promoter-associated enhancer that exhibits looser chromatin organization and higher BRCA1 binding signal is highlighted by purple background. ShB1, shBRCA1.
Article Snippet: The following antibodies were used:
Techniques: Expressing, Quantitative Proteomics, Biomarker Discovery, Binding Assay