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PPARG  Gene / cDNA Clone

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PPARG Related Area

PPARG Related Pathways

    PPARG Summary & Protein Information

    PPARG Background

    Gene Summary: PPARG gene encodes a member of the peroxisome proliferator-activated receptor (PPAR) subfamily of nuclear receptors. PPARs form heterodimers with retinoid X receptors (RXRs) and these heterodimers regulate transcription of various genes. Three subtypes of PPARs are known: PPAR-alpha, PPAR-delta, and PPAR-gamma. The protein encoded by this PPARG gene is PPAR-gamma and is a regulator of adipocyte differentiation. Additionally, PPARG protein has been implicated in the pathology of numerous diseases including obesity, diabetes, atherosclerosis and cancer. Alternatively spliced transcript variants that encode different isoforms have been described. [provided by RefSeq, Jul 2008]
    General information above from NCBI
    Enzyme regulation: ENZYME REGULATION: PDPK1 activates its transcriptional activity independently of its kinase activity. {ECO:0000269|PubMed:16150867}.
    Subunit structure: Interacts with FOXO1 (acetylated form) (By similarity). Heterodimer with other nuclear receptors, such as RXRA. The heterodimer with the retinoic acid receptor RXRA is called adipocyte-specific transcription factor ARF6. Interacts with NCOA6 coactivator, leading to a strong increase in transcription of target genes. Interacts with coactivator PPARBP, leading to a mild increase in transcription of target genes. Interacts with NOCA7 in a ligand-inducible manner. Interacts with NCOA1 and NCOA2 LXXLL motifs. Interacts with ASXL1, ASXL2, DNTTIP2, FAM120B, MAP2K1/MEK1, NR0B2, PDPK1, PRDM16, PRMT2 and TGFB1I1. Interacts (when activated by agonist) with PPP5C. Interacts with HELZ2 and THRAP3; the interaction stimulates the transcriptional activity of PPARG. Interacts with PER2, the interaction is ligand dependent and blocks PPARG recruitment to target promoters. Interacts with CCRN4L/NOC. Interacts with ACTN4. {ECO:0000250, ECO:0000269|PubMed:10681503, ECO:0000269|PubMed:11587644, ECO:0000269|PubMed:11971969, ECO:0000269|PubMed:12039952, ECO:0000269|PubMed:12672231, ECO:0000269|PubMed:15047147, ECO:0000269|PubMed:15056000, ECO:0000269|PubMed:15258145, ECO:0000269|PubMed:15687259, ECO:0000269|PubMed:15974597, ECO:0000269|PubMed:15976031, ECO:0000269|PubMed:16150867, ECO:0000269|PubMed:16239304, ECO:0000269|PubMed:16451087, ECO:0000269|PubMed:16640330, ECO:0000269|PubMed:16919947, ECO:0000269|PubMed:17101779, ECO:0000269|PubMed:21047783, ECO:0000269|PubMed:22351778, ECO:0000269|PubMed:23525231, ECO:0000269|PubMed:9744270}.
    Subcellular location: Nucleus. Cytoplasm. Note=Redistributed from the nucleus to the cytosol through a MAP2K1/MEK1-dependent manner. CCRN4L/NOC enhances its nuclear translocation.
    Tissue specificity: Highest expression in adipose tissue. Lower in skeletal muscle, spleen, heart and liver. Also detectable in placenta, lung and ovary. {ECO:0000269|PubMed:9065481}.
    Post-translational: O-GlcNAcylation at Thr-84 reduces transcriptional activity in adipocytes. {ECO:0000250}.; Phosphorylated in basal conditions and dephosphorylated when treated with the ligand. May be dephosphorylated by PPP5C. The phosphorylated form may be inactive and dephosphorylation at Ser-112 induces adipogenic activity (By similarity). {ECO:0000250}.
    Involvement in disease: DISEASE: Note=Defects in PPARG can lead to type 2 insulin-resistant diabetes and hyptertension. PPARG mutations may be associated with colon cancer.; DISEASE: Obesity (OBESITY) [MIM:601665]: A condition characterized by an increase of body weight beyond the limitation of skeletal and physical requirements, as the result of excessive accumulation of body fat. {ECO:0000269|PubMed:9753710}. Note=Disease susceptibility may be associated with variations affecting the gene represented in this entry.; DISEASE: Lipodystrophy, familial partial, 3 (FPLD3) [MIM:604367]: A form of lipodystrophy characterized by marked loss of subcutaneous fat from the extremities. Facial adipose tissue may be increased, decreased or normal. Affected individuals show an increased preponderance of insulin resistance, diabetes mellitus and dyslipidemia. {ECO:0000269|PubMed:11788685, ECO:0000269|PubMed:12453919}. Note=The disease is caused by mutations affecting the gene represented in this entry.; DISEASE: Glioma 1 (GLM1) [MIM:137800]: Gliomas are benign or malignant central nervous system neoplasms derived from glial cells. They comprise astrocytomas and glioblastoma multiforme that are derived from astrocytes, oligodendrogliomas derived from oligodendrocytes and ependymomas derived from ependymocytes. Note=Disease susceptibility may be associated with variations affecting the gene represented in this entry. Polymorphic PPARG alleles have been found to be significantly over-represented among a cohort of American patients with sporadic glioblastoma multiforme suggesting a possible contribution to disease susceptibility.
    Sequence similarity: Belongs to the nuclear hormone receptor family. NR1 subfamily. {ECO:0000305}.; Contains 1 nuclear receptor DNA-binding domain. {ECO:0000255|PROSITE-ProRule:PRU00407}.
    General information above from UniProt

    PPARG Alternative Name

    GLM1,CIMT1,NR1C3,PPARG1,PPARG2,PPARgamma, [homo-sapiens]
    CIMT1,GLM1,NR1C3,PPARG1,PPARG2,PPARgamma, [human]
    PPARgamma2,Nr1c3,PPARgamma,PPAR-gamma,PPAR-gamma2, [mouse]
    Nr1c3,PPARgamma,PPAR-gamma,PPARgamma2,PPAR-gamma2, [mus-musculus]

    PPARG Related Studies

  • Hamblin M, et al. (2009) PPARs and the Cardiovascular System. Antioxid Redox Signal. 11 (6): 1415-52.
  • Khateeb J, et al. (2010) Paraoxonase 1 (PON1) expression in hepatocytes is upregulated by pomegranate polyphenols: a role for PPAR-gamma pathway. Atherosclerosis. 208 (1): 119-25.
  • Fajas L, et al. (1997) The organization, promoter analysis, and expression of the human PPARgamma gene. J Biol Chem. 272 (30): 18779-89.