MIM/BEG4, a Sonic hedgehog-responsive gene that potentiates Gli-dependent transcription

被引：130

作者：

Callahan, CA

Ofstad, T

Horng, L

Wang, JK

Zhen, HH

Coulombe, PA

Oro, AE ^{[1
]}

机构：

[1] Stanford Univ, Sch Med, Program Epithelial Biol, Stanford, CA 94305 USA

[2] Stanford Univ, Sch Med, Dept Pathol, Stanford, CA 94305 USA

[3] Johns Hopkins Univ, Sch Med, Dept Biol Chem, Baltimore, MD 21205 USA

[4] Johns Hopkins Univ, Sch Med, Dept Dermatol, Baltimore, MD 21205 USA

来源：

GENES & DEVELOPMENT | 2004年 / 18卷 / 22期

关键词：

sonic hedgehog; Gli; MIM; BCC; actin; transcription;

D O I：

10.1101/gad.1221804

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Sonic hedgehog (Shh) signaling plays a critical role during development and carcinogenesis. While Gli family members govern the transcriptional output of Shh signaling, little is known how Gli-mediated transcriptional activity is regulated. Here we identify the actin-binding protein Missing in Metastasis (MIM) as a new Shh-responsive gene. Together, Gli1 and MIM recapitulate Shh-mediated epidermal proliferation and invasion in regenerated human skin. MIM is part of a Gli/Suppressor of Fused complex and potentiates Gli-dependent transcription using domains distinct from those used for monomeric actin binding. These data define MIM as both a Shh-responsive gene and a new member of the pathway that modulates Gli responses during growth and tumorigenesis.

引用

页码：2724 / 2729

页数：6

共 37 条

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