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受体“Ck”依赖性信号传导调节低密度脂蛋白受体基因转录。

Receptor-'Ck' dependent signalling regulates the LDL-receptor gene transcription.

作者信息

Goel R, Singh J, Kaul D

机构信息

Department of Experimental Medicine and Biotechnology, Post Graduate Institute of Medical Education and Research, Chandigarh, India.

出版信息

Mol Cell Biochem. 1997 Apr;169(1-2):79-83. doi: 10.1023/a:1006806118493.

Abstract

Evidence of a novel receptor, having affinity for cholesterol in lipoproteins and intrinsic tyrosine kinase activity (designated as Receptor 'Ck') prompted us to explore its role in LDL-dependent transcriptional regulation of apoprotein-B specific LDL receptor gene in human lymphocytes. The results of this study revealed that LDL dependent activation of this Receptor 'Ck' was essential for the regulation of apoprotein-B specific LDL receptor gene transcription. Further, by using various blockers of as well as simulating the Receptor 'Ck'-dependent signalling in human lymphocytes, we were able to show that Receptor 'Ck'-dependent signalling was involved in the LDL-dependent transcriptional regulation of 160 kDa apoprotein B specific LDL receptor gene. Based upon these results, we conclude that cholesterol derived from LDL. catabolism within the cell does not have any role in the transcriptional regulation of apoprotein B specific LDL receptor gene.

摘要

一种对脂蛋白中的胆固醇具有亲和力且具有内在酪氨酸激酶活性的新型受体(命名为受体“Ck”)的证据促使我们探索其在人淋巴细胞中载脂蛋白B特异性低密度脂蛋白受体基因的低密度脂蛋白依赖性转录调控中的作用。这项研究的结果表明,该受体“Ck”的低密度脂蛋白依赖性激活对于载脂蛋白B特异性低密度脂蛋白受体基因转录的调控至关重要。此外,通过使用各种阻滞剂以及模拟人淋巴细胞中受体“Ck”依赖性信号传导,我们能够证明受体“Ck”依赖性信号传导参与了160 kDa载脂蛋白B特异性低密度脂蛋白受体基因的低密度脂蛋白依赖性转录调控。基于这些结果,我们得出结论,细胞内低密度脂蛋白分解代谢产生的胆固醇在载脂蛋白B特异性低密度脂蛋白受体基因的转录调控中没有任何作用。

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