瘦素受体（OB-R）介导的功能性信号转导与转录激活因子1和3信号通路；转染细胞中大鼠脂肪瘦素受体表达降低。
Functional STAT 1 and 3 signaling by the leptin receptor (OB-R); reduced expression of the rat fatty leptin receptor in transfected cells.
作者信息
Rosenblum C I, Tota M, Cully D, Smith T, Collum R, Qureshi S, Hess J F, Phillips M S, Hey P J, Vongs A, Fong T M, Xu L, Chen H Y, Smith R G, Schindler C, Van der Ploeg L H
机构信息
Department of Genetics & Molecular Biology, Merck Research Laboratories, Merck & Co., Rahway, NJ 07065, USA.
出版信息
Endocrinology. 1996 Nov;137(11):5178-81. doi: 10.1210/endo.137.11.8895396.
The leptin receptor (OB-R) bears homology to members of the class I cytokine receptor family. We demonstrate that leptin binding to OB-R stimulates formation of STAT-1 and STAT-3 complexes, thereby defining transcriptional motifs for genes that are under leptin control. Transfected fa OB-R bound leptin with equal affinity to that of wild type OB-R. fa OB-R abundance was about 7 fold reduced compared to control cells. Surprisingly, the low level of fa OB-R is fully capable of activating the STAT signal transduction pathway. We discuss plausible explanations for the obese phenotype in Zucker fatty rats.
瘦素受体（OB-R）与I类细胞因子受体家族成员具有同源性。我们证明，瘦素与OB-R结合可刺激STAT-1和STAT-3复合物的形成，从而确定受瘦素调控的基因的转录基序。转染的fa OB-R与瘦素的结合亲和力与野生型OB-R相同。与对照细胞相比，fa OB-R的丰度降低了约7倍。令人惊讶的是，低水平的fa OB-R完全能够激活STAT信号转导通路。我们讨论了对Zucker肥胖大鼠肥胖表型的合理解释。
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