The antiserum was produced against synthesized peptide derived from human PPAR-gamma around the phosphorylation site of Ser112. AA range:78-127

Phospho-PPAR-γ (S112) Polyclonal Antibody detects endogenous levels of PPAR-γ protein only when phosphorylated at S112.The name of modified sites may be influenced by many factors, such as species (the modified site was not originally found in human samples) and the change of protein sequence (the previous protein sequence is incomplete, and the protein sequence may be prolonged with the development of protein sequencing technology). When naming, we will use the "numbers" in historical reference to keep the sites consistent with the reports. The antibody binds to the following modification sequence (lowercase letters are modification sites):PAsPP

PPARG

Peroxisome proliferator-activated receptor gamma

PPARG ;
NR1C3 ;
Peroxisome proliferator-activated receptor gamma ;
PPAR-gamma ;
Nuclear receptor subfamily 1 group C member 3

peroxisome proliferator activated receptor gamma (PPARG) Homo sapiens This 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 gene is PPAR-gamma and is a regulator of adipocyte differentiation. Additionally , PPAR-gamma 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] ,

Alternative products:Additional isoforms seem to exist ,Disease:Defects in PPARG are the cause of familial partial lipodystrophy type 3 (FPLD3) [MIM:604367]. Familial partial lipodystrophies (FPLD) are a heterogeneous group of genetic disorders characterized by marked loss of subcutaneous (sc) fat from the extremities. Affected individuals show an increased preponderance of insulin resistance , diabetes mellitus and dyslipidemia. ,Disease:Defects in PPARG can lead to type 2 insulin-resistant diabetes and hyptertension. ,Disease:Defects in PPARG may be associated with colon cancer. ,Disease:Defects in PPARG may be associated with susceptibility to obesity [MIM:601665]. ,Disease:Variation in PPARG is associated with carotid intimal medial thickness 1 (CIMT1) [MIM:609338]. CIMT is a measure of atherosclerosis that is independently associated with traditional atherosclerotic cardiovascular disease risk factors and coronary atherosclerotic burden. 35 to 45% of the variability in multivariable-adjusted CIMT is explained by genetic factors. ,Function:Receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand , the receptor binds to a promoter element in the gene for acyl-CoA oxidase and activates its transcription. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. ,online information:Peroxisome proliferator-activated receptor entry ,online information:The Singapore human mutation and polymorphism database ,polymorphism:Genetic variation in PPARG may influence body mass index (BMI) [MIM:606641]. BMI reflects the amount of fat , lean mass , and body build. ,similarity:Belongs to the nuclear hormone receptor family. ,similarity:Belongs to the nuclear hormone receptor family. NR1 subfamily. ,similarity:Contains 1 nuclear receptor DNA-binding domain. ,subunit:Forms a heterodimer with the retinoic acid receptor RXRA 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 FAM120B (By similarity) . Interacts with NOCA7 in a ligand-inducible manner. Interacts with NCOA1 LXXLL motifs. Interacts with TGFB1I1. Interacts with DNTTIP2. ,tissue specificity:Highest expression in adipose tissue. Lower in skeletal muscle , spleen , heart and liver. Also detectable in placenta , lung and ovary. ,

Nucleus. Cytoplasm. Redistributed from the nucleus to the cytosol through a MAP2K1/MEK1-dependent manner. NOCT enhances its nuclear translocation.

>>PPAR signaling pathway ;
>>AMPK signaling pathway ;
>>Longevity regulating pathway ;
>>Osteoclast differentiation ;
>>Thermogenesis ;
>>Non-alcoholic fatty liver disease ;
>>Huntington disease ;
>>Pathways in cancer ;
>>Transcriptional misregulation in cancer ;
>>Thyroid cancer ;
>>Lipid and atherosclerosis