Abstract
Sonic hedgehog (Shh) signaling plays a critical role during development and carcinogens. 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.
Original language | English (US) |
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Pages (from-to) | 2724-2729 |
Number of pages | 6 |
Journal | Genes and Development |
Volume | 18 |
Issue number | 22 |
DOIs | |
State | Published - Nov 15 2004 |
Externally published | Yes |
Keywords
- Actin
- BCC
- Gli
- MIM
- Sonic hedgehog
- Transcription
ASJC Scopus subject areas
- Genetics
- Developmental Biology