Journal
CELLULAR SIGNALLING
Volume 25, Issue 6, Pages 1526-1538Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2012.12.025
Keywords
SASH1; Mutation; Melanocyte migration; G alpha s; IQGAP1
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Funding
- National Natural Science Foundation of China [30971582, 90919049]
- Ministry of Science and Technology of China 973 Program [2010CB529600, 2009CB825606]
- Shanghai Municipal Commission of Science and Technology Program [09DJ1400601]
- excellent cross-disciplinary doctoral research funding schemes of Fudan University
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One important function of melanocytes (MCs) is to produce and transfer melanin to neighbouring keratinocytes (KCs) to protect epithelial cells from UV radiation. The mechanisms regulating the specific migration and localisation of the MC lineage remain unknown. We have found three heterozygous mutations that cause amino add substitutions in the SASH1 gene in individuals with a kind of dyschromatosis. In epidermal tissues from an affected individual, we observed the increased transepithelial migration of melanocytes. Functional analyses indicate that these SASH1 mutations not only cause the increased migration of A375 cells and but also induce intensive bindings with two novel cell adhesion partners IQGAP1 and G alpha s. Further, SASH1 mutations induce uniform loss of E-Cadherin in human A375 cells. Our findings suggest a new scaffold protein SASH1 to regulate IQGAP1-E-Cadherin signalling and demonstrate a novel crosstalking between GPCR signalling, calmodulin signalling for the modulation of MCs invasion. (C) 2013 Elsevier Inc. All rights reserved.
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