MIM/BEG4, a Sonic hedgehog-responsive gene that potentiates Gli-dependent transcription
Copyright policy )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.
- Stanford University United States
- Johns Hopkins University United States
Mice, Knockout, Gene Expression Profiling, Microfilament Proteins, Kruppel-Like Transcription Factors, Nuclear Proteins, Fibroblasts, Embryo, Mammalian, Actins, Neoplasm Proteins, Mice, Epidermal Cells, Animals, Humans, Immunoprecipitation, Hedgehog Proteins, Neoplasm Invasiveness, Epidermis, Cell Division, In Situ Hybridization, Oligonucleotide Array Sequence Analysis
Mice, Knockout, Gene Expression Profiling, Microfilament Proteins, Kruppel-Like Transcription Factors, Nuclear Proteins, Fibroblasts, Embryo, Mammalian, Actins, Neoplasm Proteins, Mice, Epidermal Cells, Animals, Humans, Immunoprecipitation, Hedgehog Proteins, Neoplasm Invasiveness, Epidermis, Cell Division, In Situ Hybridization, Oligonucleotide Array Sequence Analysis
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