PPAR-γ Rabbit mAb

Human,Mouse

WB,IHC,IF,IP,ELISA

单克隆抗体

PPARG

Peroxisome proliferator-activated receptor gamma

58kD

Endogenous

PBS, 50% glycerol, 0.05% Proclin 300, 0.05%BSA

Monoclonal, Rabbit,IgG

IHC 1:500-1:1000; WB 1:2000-1:10000; IF 1:200-1:1000; ELISA 1:5000-1:20000; IP 1:50-1:200; Note: For IHC, we suggest antigen retrieval with TE buffer pH 9.0

Protein A

0.5 mg/ml

-15°C to -25°C/1 year(Do not lower than -25°C)

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

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.,