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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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

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.[1]

References

  1. MIM/BEG4, a Sonic hedgehog-responsive gene that potentiates Gli-dependent transcription. Callahan, C.A., Ofstad, T., Horng, L., Wang, J.K., Zhen, H.H., Coulombe, P.A., Oro, A.E. Genes Dev. (2004) [Pubmed]
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