HCSGD entry for PPARGC1A

1. General information

Official gene symbolPPARGC1A
Entrez ID10891
Gene full nameperoxisome proliferator-activated receptor gamma, coactivator 1 alpha
Other gene symbolsLEM6 PGC-1(alpha) PGC-1v PGC1 PGC1A PPARGC1
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000166Nucleotide bindingIEAmolecular_function
GO:0001104RNA polymerase II transcription cofactor activityTASmolecular_function
GO:0001659Temperature homeostasisTASbiological_process
GO:0001678Cellular glucose homeostasisNASbiological_process
GO:0003677DNA bindingISS TASmolecular_function
GO:0003713Transcription coactivator activityIDAmolecular_function
GO:0003723RNA bindingTASmolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005634NucleusIDA ISS TAScellular_component
GO:0005654NucleoplasmTAScellular_component
GO:0005665DNA-directed RNA polymerase II, core complexTAScellular_component
GO:0005829CytosolIEAcellular_component
GO:0006012Galactose metabolic processIEAbiological_process
GO:0006094GluconeogenesisNASbiological_process
GO:0006355Regulation of transcription, DNA-templatedIDAbiological_process
GO:0006367Transcription initiation from RNA polymerase II promoterTASbiological_process
GO:0006397MRNA processingTASbiological_process
GO:0006461Protein complex assemblyTASbiological_process
GO:0007005Mitochondrion organizationNASbiological_process
GO:0007586DigestionTASbiological_process
GO:0008134Transcription factor bindingTASmolecular_function
GO:0008209Androgen metabolic processIEAbiological_process
GO:0008380RNA splicingTASbiological_process
GO:0009409Response to coldIEAbiological_process
GO:0010822Positive regulation of mitochondrion organizationISSbiological_process
GO:0010941Regulation of cell deathIDAbiological_process
GO:0014850Response to muscle activityISSbiological_process
GO:0016605PML bodyIEAcellular_component
GO:0016922Ligand-dependent nuclear receptor bindingIPImolecular_function
GO:0019395Fatty acid oxidationNASbiological_process
GO:0022904Respiratory electron transport chainISSbiological_process
GO:0030374Ligand-dependent nuclear receptor transcription coactivator activityIDAmolecular_function
GO:0030521Androgen receptor signaling pathwayNASbiological_process
GO:0031490Chromatin DNA bindingISSmolecular_function
GO:0034599Cellular response to oxidative stressISSbiological_process
GO:0035066Positive regulation of histone acetylationTASbiological_process
GO:0036273Response to statinIEAbiological_process
GO:0042594Response to starvationNASbiological_process
GO:0043201Response to leucineIEAbiological_process
GO:0043524Negative regulation of neuron apoptotic processISSbiological_process
GO:0043565Sequence-specific DNA bindingIDAmolecular_function
GO:0045333Cellular respirationTASbiological_process
GO:0045722Positive regulation of gluconeogenesisTASbiological_process
GO:0045820Negative regulation of glycolysisIEAbiological_process
GO:0045893Positive regulation of transcription, DNA-templatedIDA NASbiological_process
GO:0045944Positive regulation of transcription from RNA polymerase II promoterISSbiological_process
GO:0046321Positive regulation of fatty acid oxidationTASbiological_process
GO:0048661Positive regulation of smooth muscle cell proliferationIEAbiological_process
GO:0050681Androgen receptor bindingNASmolecular_function
GO:0050821Protein stabilizationTASbiological_process
GO:0050873Brown fat cell differentiationTASbiological_process
GO:0051091Positive regulation of sequence-specific DNA binding transcription factor activityIDAbiological_process
GO:0051552Flavone metabolic processIEAbiological_process
GO:0070997Neuron deathIDAbiological_process
GO:0071250Cellular response to nitriteIEAbiological_process
GO:0071356Cellular response to tumor necrosis factorIEAbiological_process
GO:0071398Cellular response to fatty acidIEAbiological_process
GO:0071456Cellular response to hypoxiaIEAbiological_process
GO:0071871Response to epinephrineIEAbiological_process
GO:0071873Response to norepinephrineIEAbiological_process
GO:0097067Cellular response to thyroid hormone stimulusIEAbiological_process
GO:1901857Positive regulation of cellular respirationIEAbiological_process
GO:1901860Positive regulation of mitochondrial DNA metabolic processIEAbiological_process
GO:1901863Positive regulation of muscle tissue developmentIEAbiological_process
GO:2000272Negative regulation of receptor activityIEAbiological_process
GO:2000310Regulation of N-methyl-D-aspartate selective glutamate receptor activityIEAbiological_process
GO:2000507Positive regulation of energy homeostasisISSbiological_process
GO:2001171Positive regulation of ATP biosynthetic processISSbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.08406895250.74733411340.60990467801.0000000000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Up0.0975213189
GSE13712_SHEARUp0.0577993822
GSE13712_STATICDown-0.0508097604
GSE19018Up0.0440108381
GSE19899_A1Up0.1976276289
GSE19899_A2Down-0.0393555255
PubMed_21979375_A1Up0.3214165762
PubMed_21979375_A2Up0.1898030555
GSE35957Down-0.1215395580
GSE36640Up0.0028438708
GSE54402Up0.1510441426
GSE9593Down-0.4655490195
GSE43922Up0.3762101250
GSE24585Down-0.4423589017
GSE37065Up1.1139618427
GSE28863_A1Up0.4499565552
GSE28863_A2Up0.6585877187
GSE28863_A3Up0.0988683954
GSE28863_A4Up0.0014655717
GSE48662Down-0.1890555727

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-23a-3pMIMAT0000078MIRT006280Luciferase reporter assayFunctional MTI22318941
hsa-miR-335-5pMIMAT0000765MIRT017345MicroarrayFunctional MTI (Weak)18185580
hsa-miR-98-5pMIMAT0000096MIRT027602MicroarrayFunctional MTI (Weak)19088304
hsa-miR-421MIMAT0003339MIRT039358CLASHFunctional MTI (Weak)23622248
hsa-miR-425-3pMIMAT0001343MIRT042423CLASHFunctional MTI (Weak)23622248
hsa-miR-378a-5pMIMAT0000731MIRT043961CLASHFunctional MTI (Weak)23622248
hsa-let-7b-5pMIMAT0000063MIRT051970CLASHFunctional MTI (Weak)23622248
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  • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 13 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

28096886Expression of SIRT1, p21, and PGC-1alpha was determined by western blot
28096886Further assays showed upregulation of SIRT1 and PGC-1alpha and downregulation of p21 after STL treatment
27221886PGC-1alpha expression was repressed after carbion-ion irradiation, and hTERT inhibition by MST-312 could further exacerbate this effect
26923269Over the last decade, extensive studies have demonstrated that SIRT1 can activate several transcriptional factors, such as peroxisome proliferator activated receptor gamma co-activator 1alpha (PGC-1alpha) and hypoxia-inducible factor 1alpha (HIF-1alpha) resulting in ameliorated mitochondria biogenesis and extended life span
26414604A recent report from Xiong and colleagues demonstrates a pivotal role for the transcription co-factor peroxisome proliferator-activated receptor gamma co-activator-1alpha (PGC-1alpha) in maintaining TERT expression and preventing vascular senescence and atherosclerosis in mice
26414604Ablation of PGC-1alpha reduced TERT expression and increased DNA damage and reactive oxygen species (ROS), resulting in shortened telomeres and vascular senescence
26414604In the ApoE(-/-) mouse model of atherosclerosis, forced expression of PGC-1alpha increased expression of TERT, extended telomeres, and reversed genomic DNA damage, vascular senescence, and the development of atherosclerotic plaques
26414604Alpha lipoic acid (ALA) stimulated expression of PGC-1alpha and TERT and reversed DNA damage, vascular senescence, and atherosclerosis, similarly to ectopic expression of PGC-1alpha
26414604ALA stimulated cyclic adenosine monophosphate (cAMP) signaling, which in turn activated the cAMP response element-binding protein (CREB), a co-factor for PGC-1alpha expression
26299964PGC-1alpha Modulates Telomere Function and DNA Damage in Protecting against Aging-Related Chronic Diseases
26299964Here, we show that ablation of peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) accelerates vascular aging and atherosclerosis, coinciding with telomere dysfunction and shortening and DNA damage
26299964PGC-1alpha deletion reduces expression and activity of telomerase reverse transcriptase (TERT) and increases p53 levels
26299964Ectopic expression of PGC-1alpha coactivates TERT transcription and reverses telomere malfunction and DNA damage
26299964These results illustrate the pivotal importance of PGC-1alpha in ameliorating senescence, aging, and associated chronic diseases, and may inform novel therapeutic approaches involving electrophilic specificity
25148910However, levels of SIRT1 and its downstream target PGC-1alpha were found to increase with age and compensatory performance
24729935Studies have identified alterations in the level or activity of factors such as SIRT1, PGC-1alpha, HIF-1alpha and c-MYC involved in key regulatory processes in the maintenance of mitochondrial structural integrity, biogenesis and function
23788763OBJECTIVE: Peroxisome proliferator-activated receptor gamma, coactivator 1alpha (PGC-1alpha) is an important mediator of mitochondrial biogenesis and function
23788763Because dysfunctional mitochondria might be involved in the pathogenesis of vascular disease, the current study was designed to investigate the effects of in vivo PGC-1alpha deficiency during chronic angiotensin II (ATII) treatment
237887631 mg/kg per day for 7 days) did not cause vascular dysfunction in wild-type mice, it led to impaired endothelial-dependent and endothelial-independent relaxation in PGC-1alpha knockout mice
23788763In parallel, oxidative stress was increased in aortic rings from ATII-treated PGC-1alpha knockout mice, whereas no change in nitric oxide production was observed
23788763In vivo treatment with the mitochondria-targeted antioxidant Mito-TEMPO partially corrected endothelial dysfunction and prevented vascular inflammation in ATII-treated PGC-1alpha mice, suggesting a causative role of mitochondrial reactive oxygen species in this setting
23788763CONCLUSIONS: PGC-1alpha deletion induces vascular dysfunction and inflammation during chronic ATII infusion by increasing mitochondrial reactive oxygen species production
23430617Peroxisome proliferator-activated receptor gamma coactivator-1alpha (PGC-1alpha) is a master regulator of mitochondrial biogenesis and function, oxidative stress, and insulin resistance
23430617Senescence is associated with telomere and mitochondrial dysfunction and oxidative stress, implying a potential causal role of PGC-1alpha in senescence pathogenesis
23430617APPROACH AND RESULTS: We generated a PGC-1alpha(+/-)/apolipoprotein E(-/-) mouse model and showed that PGC-1alpha deficiency promotes a vascular senescence phenotype that is associated with increased oxidative stress, mitochondrial abnormalities, and reduced telomerase activity
23430617PGC-1alpha disruption results in reduced expression of the longevity-related deacetylase sirtuin 1 (SIRT1) and the antioxidant catalase, and increased expression of the senescence marker p53 in aortas
23430617Further, angiotensin II, a major hormonal inducer of vascular senescence, induces prolonged lysine acetylation of PGC-1alpha and releases the PGC-1alpha-FoxO1 complex from the SIRT1 promoter, thus reducing SIRT1 expression
23430617The phosphorylation-defective mutant PGC-1alpha S570A is not acetylated, is constitutively active for forkhead box O1-dependent SIRT1 transcription, and prevents angiotensin II-induced senescence
23430617Acetylation of PGC-1alpha by angiotensin II interrupts the PGC-1alpha-forkhead box O1-SIRT1 feed-forward signaling circuit leading to SIRT1 and catalase downregulation and vascular senescence
23430617CONCLUSIONS: PGC-1alpha is a primary negative regulator of vascular senescence
23430617Moreover, the central role of posttranslational modification of PGC-1alpha in regulating angiotensin II-induced vascular senescence may inform development of novel therapeutic strategies for mitigating age-associated diseases, such as atherosclerosis
23159434The effect of overexpression of PGC-1alpha on the mtDNA4834 common deletion in a rat cochlear marginal cell senescence model
23159434Previous researches have shown that peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) is a key regulator of mitochondrial biogenesis and energy metabolism
23159434However, the expression of PGC-1alpha in the inner ear and the possible effect of PGC-1alpha on presbycusis are not clear
23159434We also found that PGC-1alpha and its downstream transcription factors compensatorily increased in our cell senescence model
23159434Furthermore, the overexpression of PGC-1alpha induced by transfection largely increased the expression levels of NRF-1 and TFAM and significantly decreased the expression level of NF-kappaB in the cell senescence model
23159434And the levels of CD, senescent cells and apoptotic cells in the cell model decreased after PGC-1alpha overexpression
23022608This was accompanied by an increase in mitochondrial mass detected by mitotracker green staining, an increased expression of the peroxisome proliferator-activated receptor gamma (PPARgamma) coactivator 1-alpha (PGC-1alpha) and succinate dehydrogenase activity as detected by MTT
22868792This is mainly due to the lack of reactivity of proliferator-activated receptor-gamma (PPAR-gamma) coactivator 1alpha (PGC-1alpha) in old animals
22868792PGC-1alpha acts as a master regulator of energy metabolism and mitochondrial biogenesis and recent evidence shows that it interacts with p53 and telomerase
15914121PGC-1alpha regulates the mitochondrial antioxidant defense system in vascular endothelial cells
15914121We postulated that a transcriptional coactivator, peroxisome proliferator activated receptor-gamma coactivator 1alpha (PGC-1alpha), a major regulator of oxidative metabolism and mitochondrial biogenesis, could be involved in the transcriptional regulation of the mitochondrial antioxidant defense system in vascular endothelial cells
15914121METHODS AND RESULTS: We show that PGC-1alpha is present in human, bovine, and mouse endothelial cells and positively modulates the expression of the mitochondrial detoxification system
15914121Endothelial cells that overexpress PGC-1alpha show reduced accumulation of reactive oxygen species (ROS), increased mitochondrial membrane potential, and reduced apoptotic cell death both in basal and oxidative stress conditions
15914121Downregulation of PGC-1alpha levels by siRNA reduces the expression of mitochondrial detoxification proteins
15914121In addition, they suggest that PGC-1alpha could play a crucial protective role in vascular complications of diabetes, where the mitochondrial metabolism of glucose has been shown to result in oxidative stress and vascular endothelial cell dysfunction
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