Reference - Detail
|Author||Yamashita T, Murakami T, Otani S, Kuwajima M, Shima K.|
|Title||Leptin receptor signal transduction: OBRa and OBRb of fa type.|
|Journal||Biochem. Biophys. Res. Commun.|
We report herein the characterization of activities of signal transduction for three types of leptin receptors (OBRs) from rats, the OBRa, OBRb, and OBRb with fa mutation (OBRb-fa), by measurement of the levels of tyrosine phosphorylation of STAT3 (signal transducers and activators of transcription 3) and MAPK (mitogen-activated protein kinase), which are induced by leptin stimulation of CHO cells stably expressing the OBR (CHO-OBRb, CHO-OBRa, or CHO-OBRb-fa cells). As the result of leptin stimulation, enhanced levels of tyrosine phosphorylation of STAT3 and MAPK were detected in CHO-OBRb cells. In CHO-OBRb-fa cells, enhancement levels for both were lower than those in CHO-OBRb cells. In CHO-OBRa cells, only the phosphorylation of MAPK was detected. These data suggest that these reduced signaling activities cause obesity in fa/fa rats and that OBRa, which has been generally thought to be inactive at signaling, actually transmits signals through the MAPK pathway.
|MeSH||Animals CHO Cells Calcium-Calmodulin-Dependent Protein Kinases / metabolism Carrier Proteins / classification Carrier Proteins / genetics Carrier Proteins / metabolism* Cricetinae DNA-Binding Proteins / metabolism Enzyme Activation Gene Expression Regulation Leptin MAP Kinase Kinase 1 Mitogen-Activated Protein Kinase Kinases* Mutation Phosphorylation Protein-Serine-Threonine Kinases / antagonists & inhibitors Protein-Tyrosine Kinases / antagonists & inhibitors Proteins / metabolism* Rats Receptors, Cell Surface* Receptors, Cytokine / classification Receptors, Cytokine / genetics Receptors, Cytokine / metabolism* Receptors, Leptin Recombinant Proteins / metabolism STAT3 Transcription Factor Signal Transduction Trans-Activators / metabolism Transcription, Genetic|
|WOS Category||BIOPHYSICS BIOCHEMISTRY & MOLECULAR BIOLOGY|
|DNA material||465.20 Mouse JunB (RDB01298)|