期刊
FEBS LETTERS
卷 585, 期 14, 页码 2187-2192出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.febslet.2011.05.060
关键词
CACNG; Claudin; N-glycosylation; Morpholino; Cataract
资金
- Fight for Sight [1658]
- Newlife Foundation for Disabled Children
- National Eye Research Centre [SCIAD 051]
- Manchester Biomedical Research Centre
- Manchester Academic Health Sciences Centre (MAHSC)
- National Institute for Health Research (NIHR)
- Biotechnology and Biological Sciences Research Council
- Wellcome Trust
- University of Manchester
A novel gene, TMEM114, was annotated as a member of the claudin gene family and was subsequently associated as a cause of autosomal dominant cataract because of a translocation in its putative promoter. Our bioinformatic and molecular analyses of TMEM114, and the closely related TMEM235, demonstrate that these proteins are more closely related to members of the voltage dependent calcium channel gamma subunit family. TMEM114 and TMEM235 differed from claudins in terms of localisation in polarised epithelial cells and by the presence of N-linked glycans. By gene expression knockdown in Xenopus tropicalis we also demonstrate a role for Tmem114 in eye development. Structured summary of protein interactions: Claudin-2 and ZO-1 colocalize by fluorescence microscopy (View interaction). ZO-1 and Tmem114 colocalize by fluorescence microscopy (View interaction). (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
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