Functional interaction of an axin homolog, conductin, with β-catenin, APC, and GSK3β

被引：1094

作者：

Behrens, J

Jerchow, BA

Würtele, M

Grimm, J

Asbrand, C

Wirtz, R

Kühl, M

Wedlich, D

Birchmeier, W

机构：

[1] Max Delbruck Ctr Mol Med, D-13122 Berlin, Germany

[2] Univ Ulm, D-89081 Ulm, Germany

来源：

SCIENCE | 1998年 / 280卷 / 5363期

关键词：

D O I：

10.1126/science.280.5363.596

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Control of stability of beta-catenin is central in the wnt signaling pathway. Here, the protein conductin was found to form a complex with both beta-catenin and the tumor suppressor gene product adenomatous polyposis coli (APC), Conductin induced beta-catenin degradation, whereas mutants of conductin that were deficient in complex formation stabilized beta-catenin. Fragments of APC that contained a conductin-binding domain also blocked beta-catenin degradation. Thus, conductin is a component of the multiprotein complex that directs beta-catenin to degradation and is located downstream of APC. In Xenopus embryos, conductin interfered with wnt-induced axis formation.

引用

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页码：596 / 599

页数：4

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