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HDAC5 Depletion Promotes Hyper-Acetylation of FOXA1 and Potentiating HIF1α Transcriptional Activation in Pancreatic Cancer [ATAC-Seq]

GSE285080 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 6 samples Submitted 2026/02/28 Platform GPL11154
Summary
Unlike class I Histone deacetylase (HDAC) members (HDAC1, 2, 3, etc.), HDAC5, a class IIa HDAC member, is downregulated in multiple solid tumors, including pancreatic cancer, and its loss is associated with unfavorable prognosis. We observed that HDAC5 mediates FOXA1-K270 deacetylation and represses HIF1α signaling via FOXA1. To further validate our hypothesis, we performed the ATAC-seq in control and HDAC5 knockdown PANC-1 cells to test whether HDAC5 knockdown affects chromatin accessibility.
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Also filed as BioProject PRJNA1201154 and SRA study SRP552996. Searching any of these in the dataset finder brings you back here.

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