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MIM/BEG4, a Sonic hedgehog-responsive gene that potentiates Gli-dependent transcription GENES & DEVELOPMENT Callahan, C. A., Ofstad, T., Horng, L., Wang, J. K., Zhen, H. H., Coulombe, P. A., Oro, A. E. 2004; 18 (22): 2724-2729

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.

View details for DOI 10.1101/gad.1221804

View details for Web of Science ID 000225170900004

View details for PubMedID 15545630

View details for PubMedCentralID PMC528890