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

@article{citeulike:197626, 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.}, address = {Program in Epithelial Biology and Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA.}, author = {Callahan, C. A. and Ofstad, T. and Horng, L. and Wang, J. K. and Zhen, H. H. and Coulombe, P. A. and Oro, A. E.}, citeulike-article-id = {197626}, citeulike-linkout-0 = {http://dx.doi.org/10.1101/gad.1221804}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/15545630}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=15545630}, day = {15}, doi = {10.1101/gad.1221804}, issn = {0890-9369}, journal = {Genes Dev}, keywords = {gli, hedgehog, mim, shh}, month = {November}, number = {22}, pages = {2724--2729}, posted-at = {2005-05-12 22:26:47}, priority = {2}, title = {MIM/BEG4, a Sonic hedgehog-responsive gene that potentiates Gli-dependent transcription.}, url = {http://dx.doi.org/10.1101/gad.1221804}, volume = {18}, year = {2004} }

TY - JOUR ID - citeulike:197626 L3 - citeulike-article-id:197626 N2 - 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. IS - 22 JF - Genes Dev SN - 0890-9369 AD - Program in Epithelial Biology and Department of Pathology, Stanford University School of Medicine, Stanford, California 94305, USA. EP - 2729 TI - MIM/BEG4, a Sonic hedgehog-responsive gene that potentiates Gli-dependent transcription. VL - 18 SP - 2724 KW - gli KW - hedgehog KW - mim KW - shh AU - Callahan, CA AU - Ofstad, T AU - Horng, L AU - Wang, JK AU - Zhen, HH AU - Coulombe, PA AU - Oro, AE PY - 2004/11/15/ UR - http://dx.doi.org/10.1101/gad.1221804 ER -