| Literature DB >> 25752541 |
Jianyun Nie1, Chao Xu2, Jing Jin3, Juliette A Aka4, Wolfram Tempel2, Vivian Nguyen3, Linya You4, Ryan Weist4, Jinrong Min5, Tony Pawson6, Xiang-Jiao Yang7.
Abstract
Peptide motifs are often used for protein-protein interactions. We have recently demonstrated that ankyrin repeats of ANKRA2 and the paralogous bare lymphocyte syndrome transcription factor RFXANK recognize PxLPxL/I motifs shared by megalin, three histone deacetylases, and RFX5. We show here that that CCDC8 is a major partner of ANKRA2 but not RFXANK in cells. The CCDC8 gene is mutated in 3M syndrome, a short-stature disorder with additional facial and skeletal abnormalities. Two other genes mutated in this syndrome encode CUL7 and OBSL1. While CUL7 is a ubiquitin ligase and OBSL1 associates with the cytoskeleton, little is known about CCDC8. Binding and structural analyses reveal that the ankyrin repeats of ANKRA2 recognize a PxLPxL motif at the C-terminal region of CCDC8. The N-terminal part interacts with OBSL1 to form a CUL7 ligase complex. These results link ANKRA2 unexpectedly to 3M syndrome and suggest novel regulatory mechanisms for histone deacetylases and RFX7.Entities:
Mesh:
Substances:
Year: 2015 PMID: 25752541 DOI: 10.1016/j.str.2015.02.001
Source DB: PubMed Journal: Structure ISSN: 0969-2126 Impact factor: 5.006