Molecule Information
General Information of the Molecule (ID: Mol01041)
Name |
Peroxisome proliferator-activated receptor gamma (PPARG)
,Rattus norvegicus
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Synonyms |
PPAR-gamma; Nuclear receptor subfamily 1 group C member 3; Nr1c3
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Molecule Type |
Protein
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Gene Name |
Pparg
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Gene ID | |||||
Location |
Primary_assembly 4: 148423194-148548468 [+]
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Sequence |
MGETLGDPPVDPEHGAFADALPMSTSQEITMVDTEMPFWPTNFGISSVDLSVMDDHSHSF
DIKPFTTVDFSSISAPHYEDIPFTRADPMVADYKYDLKLQEYQSAIKVEPASPPYYSEKT QLYNRPHEEPSNSLMAIECRVCGDKASGFHYGVHACEGCKGFFRRTIRLKLIYDRCDLNC RIHKKSRNKCQYCRFQKCLAVGMSHNAIRFGRMPQAEKEKLLAEISSDIDQLNPESADLR ALAKHLYDSYIKSFPLTKAKARAILTGKTTDKSPFVIYDMNSLMMGEDKIKFKHITPLQE QSKEVAIRIFQGCQFRSVEAVQEITEYAKNIPGFINLDLNDQVTLLKYGVHEIIYTMLAS LMNKDGVLISEGQGFMTREFLKSLRKPFGDFMEPKFEFAVKFNALELDDSDLAIFIAVII LSGDRPGLLNVKPIEDIQDNLLQALELQLKLNHPESSQLFAKVLQKMTDLRQIVTEHVQL LHVIKKTETDMSLHPLLQEIYKDLY Click to Show/Hide
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Function |
Nuclear receptor that binds peroxisome proliferators such as hypolipidemic drugs and fatty acids. Once activated by a ligand, the nuclear receptor binds to DNA specific PPAR response elements (PPRE) and modulates the transcription of its target genes, such as acyl-CoA oxidase. It therefore controls the peroxisomal beta-oxidation pathway of fatty acids. Key regulator of adipocyte differentiation and glucose homeostasis. ARF6 acts as a key regulator of the tissue-specific adipocyte P2 (aP2) enhancer. Acts as a critical regulator of gut homeostasis by suppressing NF-kappa-B-mediated proinflammatory responses. Plays a role in the regulation of cardiovascular circadian rhythms by regulating the transcription of ARNTL/BMAL1 in the blood vessels.
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Uniprot ID | |||||
Ensembl ID | |||||
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Type(s) of Resistant Mechanism of This Molecule
UAPP: Unusual Activation of Pro-survival Pathway
Drug Resistance Data Categorized by Drug
Approved Drug(s)
1 drug(s) in total
Metformin
Drug Sensitivity Data Categorized by Their Corresponding Mechanisms | ||||
Unusual Activation of Pro-survival Pathway (UAPP) | ||||
Disease Class: Type 2 diabetes mellitus | [1] | |||
Sensitive Disease | Type 2 diabetes mellitus [ICD-11: 5A11.0] | |||
Sensitive Drug | Metformin | |||
Molecule Alteration | Expression | Up-regulation |
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Experimental Note | Discovered Using In-vivo Testing Model | |||
Experiment for Molecule Alteration |
Western blotting analysis | |||
Experiment for Drug Resistance |
OGTT assay | |||
Mechanism Description | The administration of chebulagic acid significantly reduced blood glucose by increasing insulin secretion. Further,chebulagic acid treatment increased the protein expression PPAR-Gamma and GLUT4 on insulin target tissues which indicates that chebulagic acid improved insulin sensitivity. PPAR-Gamma is a type of ligand-activated nuclear transcription factor that is associated with fat differentiation, obesity, and insulin resistance. The ability of insulin to reduce blood glucose levels results from the suppression of hepatic glucose production and increased glucose uptake in muscle and adipose tissue via GLUT4. |
References
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