143 Written by Angela K. Eggleston, Stephane Larochelle & Beth Moorefield unanticipated, but the involved residues on both KRIT1 and ICAP1 are evolutionarily conserved, which points to the likely importance of this interface. Turning to the ICAP1–b1-integrin complex, the b1 tail is seen to bind ICAP1 in the canonical PTB-binding site, consistent with KRIT1 directly competing with b1-integrin for ICAP1 association, a point that is clearly demonstrated by functional analyses. In sum, this study provides a mechanistic understanding of how inactivation of KRIT1, commonly observed in association with CCMs, can result in improper integrin activation, which in turn may contribute to a leaky vasculature. (Mol. Cell doi:10.1016/j.molcel.2012.12.005, published online 10 January 2013) SL Splicing with super 8
Stephen Kowalczykowski合作论文数Department of Microbiology and Molecular Genetics, College of Biological Sciences, University of California, Davis;Cancer Center, University of California Davis Medical Center11
Stephen West合作论文数DNA Recombination and Repair Laboratory, The Francis Crick Institute6
Sadaf Shadan合作论文数4Eccleston, Alex合作论文数4Marte, Barbara合作论文数1Ritu Dhand合作论文数1Nath, Deepa合作论文数1helen george合作论文数1Lj Roman合作论文数1Lall Sabbi合作论文数1Alison Mitchell合作论文数1Rehrauer W M合作论文数1
Alain van Gool合作论文数1Peter Baumann合作论文数1E. Morton Bradbury合作论文数1
Andrzej Stasiak合作论文数Center for Integrative Genomics, Faculty of Biology and Medicine, Université de Lausanne;Swiss Institute of Bioinformatics1
Fiona E. Benson合作论文数Department of Genetics;University of Nottingham;Department of Genetics, University of Nottingham1Carol A. Parsons合作论文数1
Didier Zerbib合作论文数1
Christine Mezard合作论文数1Adelina A. Davies合作论文数1Boris Kysela合作论文数1Eric Van Dyck合作论文数1Scott D. Lauder合作论文数1
