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Selective Class IIa HDAC inhibitor alters gene expression in NRVMs

ABSTRACT: Selective Class IIa HDAC inhibitor alters gene expression in NRVMs

PROVIDER: PRJNA534100 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8942634.fastq.gz	Fastqsanger.gz
	SRR8942635.fastq.gz	Fastqsanger.gz
	SRR8942636.fastq.gz	Fastqsanger.gz
	SRR8942637.fastq.gz	Fastqsanger.gz

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Selective Class IIa HDAC inhibitor alters gene expression in NRVMs

Project description:Expression profiling of neonatl rat ventricular cardiomyocytes (NRVMs) upon the treatement of Class IIa HDAC inhibitor

2019-04-23 | GSE130150 | GEO

Gene regulation in gastrocnemius muscle of denervated mouse with HDAC4 inducible knockout or class IIa HDAC inhibitior NVS-HD1 treatment

Project description:Our class IIa HDAC inhibitor, NVS-HD1, inhibited HDAC4 with less than 1 nM potency while exhibiting >200 fold selectivity on class IIa HDACs compared to class I (HDAC1, 3, 8) and class IIb (HDAC6) HDACs, making it the most potent and selective class IIa HDAC inhibitor reported so far. We tested the efficacy of NVS-HD1 in the mouse denervation model, either alone or on the genetic background of HDAC4 whole-body inducible knockout (HDAC4 iRKO). Global gene expression changes in gastrocnemius muscles were profiled by RNAseq. In the innervated control legs, HDAC4 knockout or NVS-HD1 caused little changes in gene expression compared to WT mice. HDAC4 knockout or NVS-HD1 mainly reversed denervation induced changes and the genes regulated by them largely overlap, suggesting that NVS-HD1 is quite specific against class IIa HDACs.

2019-11-27 | GSE136627 | GEO

RNAseq data on HDAC Class IIa inhibitor (CHDI-00390576) dosed Q175 mice.

Project description:WT and Q175 heterozygous (het) mice treated orally twice a day with vehicle (10% HPβCD), and Q175 mice treated with either 30 or 100 mg/kg orally twice a day CHDI-00390576. CHDI-00390576 is a Class IIa HDAC inhibitor. Mice were dosed from 4 weeks to 6 months of age.

2017-09-23 | GSE104064 | GEO

RNAseq data on HDAC Class IIa inhibitor (CHDI-00390576) dosed R6/2 mice.

Project description:R6/2 and WT mice treated orally twice a day with vehicle (10% HPβCD), and R6/2 mice treated with either 30 or 100 mg/kg orally twice a day CHDI-00390576. CHDI-00390576 is a Class IIa HDAC inhibitor. Mice were dosed from 4 - 12 weeks of age.

2017-09-23 | GSE104086 | GEO

MYC plus class IIa HDAC inhibiton potentiates mitochondrial dysfunction in non-small cell lung cancer [I]

Project description:To evaluate potential therapeutic benefits from dual targeting of MYC and class IIa HDACs, we assessed the treatment efficacy of MYCi plus class IIa HDACi across 18 NSCLC cell lines, 10 of which demonstrated substantial reduction of cell viability upon combination treatment. RNA sequencing on treated cell lines identified large-scale transcriptional shifts facilitated by combination treatment, including suppression of MYC, cell cycle, and mitochondrial pathways. ATAC-sequencing showed chromatin structure changes in genomic regions involved in cell cycle progression and inflammatory signaling. Furthermore, G1/S arrest and elevated mitochondrial ROS levels in combination drug-treated cells were confirmed using flow cytometry. Concordant with the role of MYC as a key cell cycle regulator, MYC protein levels were decreased in the combination treatment group as compared to the vehicle or mono-treatment groups. In summary, we define here a novel drug paradigm combining MYC and class IIa HDAC inhibitors, which potentiates anti-tumor efficacy in NSCLC via MYC depletion and oxidative stress.

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MYC plus class IIa HDAC inhibiton potentiates mitochondrial dysfunction in non-small cell lung cancer [II]

2025-04-23 | GSE281766 | GEO

MYC plus class IIa HDAC inhibiton potentiates mitochondrial dysfunction in non-small cell lung cancer [III]

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MYC plus class IIa HDAC inhibiton potentiates mitochondrial dysfunction in non-small cell lung cancer [RNA-seq]

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MYC plus class IIa HDAC inhibiton potentiates mitochondrial dysfunction in non-small cell lung cancer [ATAC-seq]

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Genome-wide Analysis of Class IIa Histone Deacetylase Regulation of Hepatic Gluconeogenesis

Project description:Analysis of Class II Histone Deacetylase (HDAC) regulation of hepatic gluconeogenesis at the gene expression level. We show that in liver, Class IIa HDACs (HDAC4, 5, and 7) are all phosphorylated and excluded from the nucleus by AMPK family kinases. In response to the fasting hormone glucagon, Class IIa HDACs rapidly translocate to the nucleus where they directly bind to the promoters of gluconeogenic enzymes such as G6Pase. In turn, HDAC4/5 mediate the acute transcriptional induction of these genes via deacetylation and activation of Foxo family transcription factors. Loss of Class IIa HDACs in the murine liver results in inhibition of FOXO target genes and lowers blood glucose, resulting in increased glycogen storage. Total RNA obtained from primary hepatocytes infected with shGFP or shHDAC4 & 5 subjected to 2 or 4 hours treatment with DMSO or forskolin.

2011-09-08 | E-GEOD-20979 | biostudies-arrayexpress

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