Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of PDK4 or ACSS2 knockdown on HASMC phenotype after 7 days of treatment [RNAseq-siPDK4-siACSS2]

ABSTRACT: We find that PDK4 knockdown mimics the effect of TGFb in HASMCs, inducing SMC glycolysis and contractile gene expressions. Wherase, ACSS2 knockdown decreases glycolysis and contractile gene expressions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE288831 | GEO | 2025/09/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

TGFβ maintains smooth muscle cell contractile phenotype via PDK4-dpendent regulation of Ac-CoA production [ATAC-Seq_TGF-siPDK4]

Project description:We find that TGFβ signaling in SMCs induced ACSS2-dependent production of Ac-CoA in a PDK4-dependent manner. TGFb induces SMC contractile phenotype and glycolysis.

2025-09-01 | GSE288977 | GEO

Effect of TGFb on HASMC phenotype after 7 days of treatment

Project description:We find that TGFβ signaling in SMCs induced ACSS2-dependent production of Ac-CoA in a PDK4-dependent manner. TGFb induces SMC contractile phenotype and glycolysis.

2025-09-01 | GSE288577 | GEO

Effect of Pdk4 smooth muscle cell-specific knockout on atherosclerosis

Project description:Knockout of Pdk4 in smooth muscle cells dramatically decreased inflammation, and increased gene expressions in TGFb signaling and glycolysis in the aorta.

2025-09-01 | GSE288576 | GEO

Effect of Pdk4 smooth muscle cell-specific knockout on atherosclerosis analyzed by scRNAseq

Project description:Knockout of Pdk4 in smooth muscle cells dramatically decreased inflammation, and increased gene expressions in TGFb signaling and glycolysis in the aorta.

2025-09-01 | GSE288834 | GEO

Effect of PDK4 or ACSS2 knockdown on HASMC phenotype after 7 days of treatment [RNAseq-siPDK4-siACSS2]

Project description:Effect of PDK4 or ACSS2 knockdown on HASMC phenotype after 7 days of treatment [RNAseq-siPDK4-siACSS2]

| PRJNA1219576 | ENA

Acetyl-CoA metabolism by ACSS2 regulates neuronal histone acetylation and long-term memory [RNA-seq]

Project description:Metabolic production of acetyl-CoA has been linked to histone acetylation and gene regulation, however the mechanisms are largely unknown. We show that the metabolic enzyme acetyl-CoA synthetase 2 (ACSS2) is a critical and direct regulator of histone acetylation in neurons and of long-term mammalian memory. We observe increased nuclear ACSS2 in differentiating neurons in vitro. Genome-wide, ACSS2 binding corresponds with increased histone acetylation and gene expression of key neuronal genes. These data indicate that ACSS2 functions as a chromatin-bound co-activator to increase local concentrations of acetyl-CoA and to locally promote histone acetylation for transcription of neuron-specific genes. Remarkably, in vivo attenuation of hippocampal ACSS2 expression in adult mice impairs long-term spatial memory, a cognitive process reliant on histone acetylation. ACSS2 reduction in hippocampus also leads to a defect in upregulation of key neuronal genes involved in memory. These results reveal a unique connection between cellular metabolism and neural plasticity, and establish a link between generation of acetyl-CoA and neuronal chromatin regulation. Global survey of gene expression in CAD cells and differentiated CAD neurons following lentiviral knockdown of ACSS2 or ATP citrate lyase (ACL) (and control = scramble hairpin); survey of hippocampal gene expression changes associated with retrieval of fear memory, after ACSS2-AAV knockdown or in EGFP-AAV control (comparison of 0h vs. 1h post-memory retrieval).

2017-05-01 | E-GEOD-76853 | biostudies-arrayexpress

Expression data from PDK4 overexpressing (Ad-PDK4 infected) and control (Ad-control infected) mouse liver

Project description:We identified PDK4 as a gene with adaptive transcriptional response to chemical stress. Although PDK4 is an energy resource regulator induced by starvation, expression of other fasting-inducible genes was unaffected, indicating additional physiological role of PDK4 for liver adaptation to the chemical stress. We used microarrays to determine genes with altered transcriptional level by PDK4 overexpression. Mice were infected with Ad-control (empty adenovirus vector) or Ad-PDK4 (PDK4 overexpressing adenovirus vector) at a dose of 10^9 PFU/mouse by tail vein injection. 3 days after the infection, mice were sacrificed for RNA preparation from the liver. Ad-control infected = 4, Ad-PDK4 infected = 3. Specimens from mice of each group were pooled, and 10 ug RNA from each pool was used for cRNA synthesis.

2010-12-25 | E-GEOD-22534 | biostudies-arrayexpress

Expression data from PDK4 overexpressing (Ad-PDK4 infected) and control (Ad-control infected) mouse liver

2010-12-25 | GSE22534 | GEO

Gene expression in activated WT or PDK4 -/- CD4+ T cells

Project description:Activation of CD4+ T cells requires metabolic reprograming to sustain demands of cellular building blocks and ATP. Pyruvate dehydrogenase kinase (PDK) is an enzyme regulating pyruvate dehydrogenase complex subunit alpha 1 (PDHE1-alpha), which converts pyruvate to acetyl-CoA. Gene expression analysis of TCR-stimulated CD4+ T cells with PDK4 deletion exhibited the reduced calcium signaling and aerobic glycolysis pathway.

2022-11-01 | GSE161653 | GEO

Acetyl-CoA metabolism by ACSS2 regulates neuronal histone acetylation and long-term memory [ChIP-seq]

Project description:Metabolic production of acetyl-CoA has been linked to histone acetylation and gene regulation, however the mechanisms are largely unknown. We show that the metabolic enzyme acetyl-CoA synthetase 2 (ACSS2) is a critical and directchum regulator of histone acetylation in neurons and of long-term mammalian memory. We observe increased nuclear ACSS2 in differentiating neurons in vitro. Genome-wide, ACSS2 binding corresponds with increased histone acetylation and gene expression of key neuronal genes. These data indicate that ACSS2 functions as a chromatin-bound co-activator to increase local concentrations of acetyl-CoA and to locally promote histone acetylation for transcription of neuron-specific genes. Remarkably, in vivo attenuation of hippocampal ACSS2 expression in adult mice impairs long-term spatial memory, a cognitive process reliant on histone acetylation. ACSS2 reduction in hippocampus also leads to a defect in upregulation of key neuronal genes involved in memory. These results reveal a unique connection between cellular metabolism and neural plasticity, and establish a link between generation of acetyl-CoA and neuronal chromatin regulation. Genome-wide examination of histone H3 and H4 acetylation, as well as ACSS2 binding, in undifferentiated CAD cells and differentiated CAD neurons; background adjusted by H3 ChIP or Input.

2017-05-01 | E-GEOD-76850 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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