Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression profiling comparisons of human PBMC treated with class I/IIb or class IIa HDAC inhibitors

ABSTRACT: The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in human PBMC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE44621 | GEO | 2013/03/24

SECONDARY ACCESSION(S): PRJNA190665

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression profiling comparisons of human PBMC treated with class I/IIb or class IIa HDAC inhibitors

Project description:The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in human PBMC. Human PBMC were cultured ex vivo with a mitogenic stimulus (1 ug/ml phytohemagglutinin, PHA) for 60 hours concurrent with exposure to vehicle (DMSO), vorinostat (3 uM), or TMP195 (3 uM). In addition to the whole PBMC populations, a portion of the cultures treated with DMSO or TMP195 were used for FACS purification of mutually exclusive CD3+ (T cell), CD19+ (B cell), and CD14+ (monocyte) populations. All samples were then processed for RNA extraction, labeling, and hybridization to Affymetrix arrays. Vehicle vs. vorinostat vs. TMP195 treatments in PBMC; Vehicle vs. TMP195 treatment in CD3+, CD19+ or CD14+ cells

2013-03-24 | E-GEOD-44621 | biostudies-arrayexpress

MMTV-PyMT whole tumor gene expression with and without Class IIa HDAC inhibitor treatment

Project description:The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in the CD3+ or CD11b+ cells residing in MMTV-PyMT tumors.

2017-03-08 | GSE87163 | 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

Differential gene expression in either CD3+ lymphocytes or CD11b+ myeloid cells due to Class IIa HDAC inhibitor treatment

Project description:The aim of this study was to identify differential gene expression resulting from the inhibition of class IIa HDACs in the CD3+ or CD11b+ cells residing in MMTV-PyMT tumors.

2017-03-08 | GSE76659 | GEO

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

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

2011-09-09 | GSE20979 | GEO

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

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

Control of Th17 Cell Development Through Cooperative Transcriptional Activities of Class IIa HDAC4 and HDAC7

Project description:Histone deacetylases (HDACs) are long recognized for important functions in regulating gene transcription in biology and diseases. However, unlike for ubiquitously expressed class I HDACs, we have little mechanistic understanding of class II HDACs that have postulated tissue specific functions. Here we report that class IIa Hdac4 and Hdac7 are up-regulated in transcription through IL-6-Stat3 signaling selectively in mouse T-helper 17 (Th17) cells during lineage-specific differentiation, but not in Th1, Th2, and Treg subtypes. Genetic knockout of Hdac4 or Hdac7 established their importance for Th17 differentiation with different functional mechanisms. Hdac4 works with Th17 transcription factors JunB-Irf4-Batf for transcriptional activation of Th17 signature genes Il17a/f, whereas Hdac7 acts distinctively in concert with Aiolos/Ncor1/Hdac3 co-repressor complex for transcriptional repression of Th17 negative regulators including Il2. Pharmacological inhibition or gene knockout of Hdac4 and Hdac7 ameliorates development of T-cell transfer induced colitis and experimental autoimmune encephalomyelitis (EAE) in mice through blockage of Th17 cell development in colon and central nervous system that recapitulate inflammatory bowel diseases and multiple sclerosis in humans, respectively. Our study highlights a previously unknown distinct mechanisms of Hdac4 and Hdac7 in transcriptional control of Th17 cell development, and rationalizes a new therapeutic strategy of targeting class IIa HDAC4/7 for the treatment of Th17-related inflammatory and autoimmune diseases.

2023-02-03 | GSE144830 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data