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填补刺猬信号通路中的空白。

Patching the gaps in Hedgehog signalling.

作者信息

Rohatgi Rajat, Scott Matthew P

机构信息

Department of Developmental Biology, Howard Hughes Medical Institute, Clark Center West W252, 318 Campus Drive, Stanford University School of Medicine, Stanford, CA 94305-5439, USA.

出版信息

Nat Cell Biol. 2007 Sep;9(9):1005-9. doi: 10.1038/ncb435.

DOI:10.1038/ncb435
PMID:17762891
Abstract

The Hedgehog (Hh) pathway plays central roles in animal development and stem-cell function. Defects in Hh signalling lead to birth defects and cancer in humans. The first and often genetically damaged step in this pathway is the interaction between two membrane proteins - Patched (Ptc), encoded by a tumour suppressor gene, and Smoothened (Smo), encoded by a proto-oncogene. Recent work linking Hh signalling to sterol metabolites and protein-trafficking events at the primary cilium promises to shed light on the biochemical basis of how Patched inhibits Smoothened, and to provide new avenues for cancer treatment.

摘要

刺猬信号通路(Hh)在动物发育和干细胞功能中发挥着核心作用。Hh信号传导缺陷会导致人类出生缺陷和癌症。该信号通路中首先且常发生基因损伤的步骤是两种膜蛋白之间的相互作用,这两种膜蛋白分别是由肿瘤抑制基因编码的Patched(Ptc)和由原癌基因编码的Smoothened(Smo)。最近将Hh信号传导与初级纤毛处的固醇代谢产物和蛋白质运输事件联系起来的研究,有望阐明Patched抑制Smoothened的生化基础,并为癌症治疗提供新途径。

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