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Genes Dev. 2004 Nov 15;18(22):2724-9.

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

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1
Program in Epithelial Biology and Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA.

Abstract

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.

PMID:
15545630
PMCID:
PMC528890
DOI:
10.1101/gad.1221804
[Indexed for MEDLINE]
Free PMC Article

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