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核心蛋白聚糖通过小窝内吞作用引发表皮生长因子受体的持续性内化和降解。

Decorin evokes protracted internalization and degradation of the epidermal growth factor receptor via caveolar endocytosis.

作者信息

Zhu Jing-Xu, Goldoni Silvia, Bix Gregory, Owens Rick T, McQuillan David J, Reed Charles C, Iozzo Renato V

机构信息

Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.

出版信息

J Biol Chem. 2005 Sep 16;280(37):32468-79. doi: 10.1074/jbc.M503833200. Epub 2005 Jul 1.

Abstract

Decorin inhibits the epidermal growth factor receptor (EGFR) by down-regulating its tyrosine kinase activity, thereby blocking the growth of a variety of transformed cells and tumor xenografts. In this study we provide evidence that decorin directly binds to the EGFR causing its dimerization, internalization, and ultimately its degradation. Using various pharmacological agents to disrupt clathrin-dependent and -independent endocytosis, we demonstrate that decorin evokes a protracted internalization of the EGFR primarily via caveolar-mediated endocytosis. In contrast to EGF, decorin targets the EGFR to caveolae, but not to early or recycling endosomes. Ultimately, however, both EGF- and decorin-induced pathways converge into late endosomes/lysosomes for final degradation. Thus, we have discovered a novel biological mechanism for decorin that could explain its anti-proliferative and anti-oncogenic mode of action.

摘要

核心蛋白聚糖通过下调其酪氨酸激酶活性来抑制表皮生长因子受体(EGFR),从而阻断多种转化细胞和肿瘤异种移植物的生长。在本研究中,我们提供证据表明核心蛋白聚糖直接与EGFR结合,导致其二聚化、内化,并最终降解。使用各种药理试剂破坏网格蛋白依赖性和非依赖性内吞作用,我们证明核心蛋白聚糖主要通过小窝介导的内吞作用引起EGFR的长时间内化。与表皮生长因子(EGF)不同,核心蛋白聚糖将EGFR靶向小窝,而不是早期或再循环内体。然而,最终,EGF和核心蛋白聚糖诱导的途径都汇聚到晚期内体/溶酶体进行最终降解。因此,我们发现了一种新的核心蛋白聚糖生物学机制,这可以解释其抗增殖和抗癌作用模式。

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