Journal
GENES & DEVELOPMENT
Volume 18, Issue 22, Pages 2724-2729Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1221804
Keywords
sonic hedgehog; Gli; MIM; BCC; actin; transcription
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Funding
- NIAMS NIH HHS [K08 AR047803, R01 AR046786, P01AR44012, R01 AR46786-02, R01 AR44232, P01 AR044012, R01 AR044232] Funding Source: Medline
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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.
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