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Type 2 diabetes susceptibility gene GRK5 regulates physiological pancreatic β-cell proliferation via phosphorylation of HDAC5

ABSTRACT: Type 2 diabetes susceptibility gene GRK5 regulates physiological pancreatic β-cell proliferation via phosphorylation of HDAC5

PROVIDER: PRJNA915603 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22889215.fastq.gz	Fastqsanger.gz
	SRR22889216.fastq.gz	Fastqsanger.gz
	SRR22889217.fastq.gz	Fastqsanger.gz
	SRR22889218.fastq.gz	Fastqsanger.gz
	SRR22889219.fastq.gz	Fastqsanger.gz

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Type 2 diabetes susceptibility gene GRK5 regulates physiological pancreatic β-cell proliferation via phosphorylation of HDAC5

Project description:Diabetes onset is accompanied with β-cell deficiency, and thus restoring functional β-cell mass is a promising therapy for those with diabetes. However, the mechanisms of β-cell mass regulation are not fully understood. Previously, we demonstrated that Sox4 is required for β-cell proliferation during prediabetes. Here, we report that Sox4 regulates β-cell mass through modulating expression of the type 2 susceptibility gene GRK5. Newly generated β-cell specific Grk5 knockout mice showed impaired glucose tolerance with reduced β-cell mass. In agreement with this phenotype, cell cycle inhibitor genes, Cdkn1a and Ccng1 were upregulated in Grk5 knockout islets. Furthermore, we found that Grk5 positively regulates β-cell mass through phosphorylation of HDAC5 and subsequent transcription of immediate early genes (IEGs) such as Nr4a1, Fosb, Junb, Arc, Egr1 and Srf. Together, these studies suggest GRK5 is linked to type 2 diabetes through regulation of β-cell mass. GRK5 could become a potential target of cell therapy to preserve functional β cells during the progression towards frank diabetes.

2023-07-31 | GSE221716 | GEO

HDAC5-ChIP seq data in HDAC5-driven KRASG12D-independent PDAC cells

Project description:HDAC5 belongs to Class IIa histone deacetylases and forms corepressor complex with HDAC3 to suppess gene expression. To identify the target genes of HDAC5, we performed ChIP-seq analysis in FLAG-tagged HDAC5 PDAC escaper cells. HDAC5 binding chromatins were pulled down by HDAC5 antibody and FLAG antibody as replicates.

2020-04-27 | GSE129549 | GEO

RNAseq data comparing HDAC5 eccaper PDAC cells with HDAC5 knockdown and scramble control

Project description:HDAC5 drives PDAC cells to bypass KRAS* dependency. To dissect the molecular mechanisms that regulated by overexpressed HDAC5 in escaper cells, we conducted RNA-seq analysis of HDAC5 escaper PDAC cells knocking down of HDAC5 or scramble shRNA control.

2020-04-27 | GSE149127 | GEO

Histone modifications regulated by HDAC5 in PDAC cells

Project description:HDAC5 belongs to Class IIa histone deacetylases and forms corepressor complex with HDAC3. To understand the epignetic regulations by HDAC5, we performed ChIP-seq analysis of H3K4me3, H3K27ac and H3K9ac in PDAC cells overexpressing GFP or HDAC5, and in HDAC5 escaper cells with HDAC5 knockdown or scramble control.

2020-04-27 | GSE149125 | GEO

HDAC5 regulates arachidonic acid metabolism via cPLA2

Project description:We performed HDAC5 knockdown in pancreatic cancer cells along with RNA sequencing. The result helped us to verify that HDAC5 regulates GATA1 dependent cPLA2 expression and arachidonic acid metabolism.

2022-10-11 | GSE185837 | GEO

HDAC5 loss impairs RB repression of oncogenic related genes and confers CDK4/6 inhibitor resistance in cancer [ChIP-seq]

Project description:The tumor suppressor protein RB acts as a transcription repressor via the interaction of its pocket domain with an L/IXCXE motif in HDAC proteins such as HDAC1. Here we demonstrated that while lacking an L/IXCXE motif, HDAC5 interacts with both RB-N (via an FXXXV motif) and RB-C segments and this interaction is diminished by RB serine-249/threonine-252 and threonine-821 phosphorylation. HDAC5 gene is frequently downregulated or deleted in human cancers such as prostate cancer. Loss of HDAC5 increases histone H3 lysine 27 acetylation (H3K27-ac) and circumvents RB-mediated repression of cell cycle-related oncogenic genes. Accordingly, HDAC5 loss confers resistance to the CDK4/6 inhibitors such as Palbociclib in prostate cancer cells in vitro and in mice, but this effect is overcome by the BET-CBP/p300 dual inhibitor NEO2734. Our findings reveal an unknown role of HDAC5 in RB-mediated histone deacetylation and gene repression and a mechanism modulating CDK4/6 inhibitor therapeutic sensitivity in cancer cells.

2021-07-24 | GSE155003 | GEO

HDAC5 loss impairs RB repression of oncogenic related genes and confers CDK4/6 inhibitor resistance in cancer [RNA-seq]

2021-07-24 | GSE155001 | GEO

HDAC5-ChIP seq data in HDAC5-driven KRASG12D-independent PDAC cells

Project description:HDAC5-ChIP seq data in HDAC5-driven KRASG12D-independent PDAC cells

| PRJNA531704 | ENA

HDAC5 is a repressor of angiogenesis and determines the angiogenic gene expression pattern of endothelial cells

Project description:Class IIa histone deacetylases (HDACs) are signal-responsive regulators of gene expression involved in vascular homeostasis. To investigate the differential role of class IIa HDACs for the regulation of angiogenesis, we used siRNA to specifically suppress the individual HDAC isoenzymes. Among the HDAC isoforms tested, silencing of HDAC5 exhibited a unique pro-angiogenic effect evidenced by increased endothelial cell migration, sprouting and tube formation. Consistently, overexpression of HDAC5 decreased sprout formation, indicating that HDAC5 is a negative regulator of angiogenesis. The anti-angiogenic activity of HDAC5 was independent of MEF2 binding and its deacetylase activity, but required a nuclear localization indicating that HDAC5 might affect the transcriptional regulation of gene expression. To identify putative HDAC5 targets, we performed microarray expression analysis. Silencing of HDAC5 increased the expression of fibroblast growth factor 2 (FGF2) and angiogenic guidance factors including Slit2. Antagonization of FGF2 or Slit2 reduced sprout induction in response to HDAC5 siRNA. ChIP assays demonstrate that HDAC5 binds to the promoter of FGF2 and Slit2. In summary, HDAC5 represses angiogenic genes, like FGF2 and Slit2, which causally contribute to capillary-like sprouting of endothelial cells. The de-repression of angiogenic genes by HDAC5 inactivation may provide a useful therapeutic target for induction of angiogenesis.

2009-04-02 | GSE15499 | GEO

RNAseq data comparing KRAS*-independent HDAC5 eccaper PDAC cells and KRAS*-dependent iKPC PDAC cells

Project description:HDAC5 drives PDAC cells to bypass KRAS* dependency. To dissect the molecular mechanisms that regulated by overexpressed HDAC5 in the bypass of KRAS* dependency, we conducted RNA-seq analysis of HDAC5 escaper PDAC cells and KRAS*-expressing iKPC PDAC cells.

2020-04-27 | GSE149126 | GEO

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