Occludin (OCLN) is an integral membrane protein, encoded by the gene mapped to human chromosome 5q13.2. OCLN is a ~65 kDa protein with four transmembrane domains including, a long COOH-terminal cytoplasmic domain, a short NH2-terminal cytoplasmic domain, two extracellular loops, and one intracellular turn. It is specifically localized at tight junctions (TJ).
Aplicação
Anti-Occludin antibody from rabbit has been used in immunocytochemistry and western blotting[1].
Ações bioquímicas/fisiológicas
Occludin (OCLN), along with tight junction (TJ)-associated peripheral membrane proteins, plays a vital role in formation and regulation of TJ. The encoded protein facilitates the translocation of p85a to TJs to regulate actin organization after oxidative stress. OCLN is also implicated in cell migration. Mutation in the gene leads to the development of band-like calcification with simplified gyration and polymicrogyria (BLC-PMG).
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Claudin-1 and -2: Novel Integral Membrane Proteins Localizing at Tight Junctions with No Sequence Similarity to Occludin.
Mikio F, et al.
The Journal of Cell Biology, 141(7), 1539?1550-1539?1550 (1998)
Recessive Mutations in the Gene Encoding the Tight Junction Protein Occludin Cause Band-like Calcification with Simplified Gyration and Polymicrogyria.
Mary C O, et al.
American Journal of Human Genetics, 87(3), 354?364-354?364 (2010)
Splicing diversity of the human OCLN gene and its biological significance for hepatitis C virus entry.
Kohaar I, et al.
Journal of Virology, 84(14), 6987-6994 (2010)
The tight junction protein, occludin, regulates the directional migration of epithelial cells.
Stem cell research & therapy, 12(1), 24-24 (2021-01-09)
Subretinal fibrosis resulting from neovascular age-related macular degeneration (nAMD) is one of the major causes of serious and irreversible vision loss worldwide, and no definite and effective treatment exists currently. Retinal pigmented epithelium (RPE) cells are crucial in maintaining the
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