Transciptome analysis of human aortic smooth muscle cells (HASMCs) with BAF60c knockdown
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ABSTRACT: HASMCs were transfected with BAF60c siRNA (siBAF60c, 20um) or control siRNA (siControl) for 48 hours, and serum-starved for 24 hours , followed by RNA-sequencing
Project description:We compared BRG1 binding and 4 histone modification states between siControl and siBAF60c transfected human aortic smooth muscle cells (HASMCs) through ChIP sequencing (ChIP-seq).
Project description:We used NGS-derived transcriptome profiling (RNA-seq) to compare the transcriptional difference between human aortic smooth muscle cells (HASMCs) transfected with 30nM siRNA targeting BAF60a (siBAF60a) or non-targeting siRNA (siControl)
Project description:We report the high-throughput RNA sequencing on human aortic smooth muscle cells (HASMCs) transfected with siRNA targeting OTUB1 (si-OTUB1) or control siRNA (si-NC). Cells were treated with PDGF-BB for 48 hours.
Project description:We compared BRG1 binding and histone modification states between siControl and siBAF60a transfected human aortic smooth muscle cells (HASMCs) through ChIP sequencing.
Project description:This research identify reduced expression of BAF60C in diabetic islets and demonstrate that altered β-cell BAF60C levels strongly influence metabolic homeostasis. Genetic loss of BAF60C in β-cells exacerbates hyperglycemia and islet dysfunction under metabolic stress, whereas β-cell–specific restoration of BAF60C produces protective effects. These findings establish BAF60C as an important regulator of β-cell integrity and disease progression in T2D.
Project description:This research identify reduced expression of BAF60C in diabetic islets and demonstrate that altered β-cell BAF60C levels strongly influence metabolic homeostasis. Genetic loss of BAF60C in β-cells exacerbates hyperglycemia and islet dysfunction under metabolic stress, whereas β-cell–specific restoration of BAF60C produces protective effects. These findings establish BAF60C as an important regulator of β-cell integrity and disease progression in T2D.
Project description:This research identify reduced expression of BAF60C in diabetic islets and demonstrate that altered β-cell BAF60C levels strongly influence metabolic homeostasis. Genetic loss of BAF60C in β-cells exacerbates hyperglycemia and islet dysfunction under metabolic stress, whereas β-cell–specific restoration of BAF60C produces protective effects. These findings establish BAF60C as an important regulator of β-cell integrity and disease progression in T2D.