Altered cellular localization and hemichannel activities of KID syndrome associated connexin26 I30N and D50Y mutations-Reference-Cited by-同舟云学术

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Altered cellular localization and hemichannel activities of KID syndrome associated connexin26 I30N and D50Y mutations

Published:2016-02-02 Issue:1 Volume:17 Page:
ISSN:1471-2121
Container-title:BMC Cell Biology
language:en
Short-container-title:BMC Cell Biol

Author:

Aypek Hande,Bay Veysel,Meşe Gülistan

Funder

The Scientific and Technological Research Council of Turkey

FP7 Marie Curie Re-Integration Grant

Publisher

Springer Science and Business Media LLC

Subject

Cell Biology

Link

http://link.springer.com/content/pdf/10.1186/s12860-016-0081-0

Reference45 articles.

1. Yeager M, Harris AL. Gap junction channel structure in the early 21st century: facts and fantasies. Curr Opin Cell Biol. 2007;19(5):521–8.

2. Goodenough DA, Paul DL. Gap junctions. Cold Spring Harbor Perspect Biol. 2009;1(1):a002576.

3. Kelly JJ, Simek J, Laird DW. Mechanisms linking connexin mutations to human diseases. Cell Tissue Res. 2015;360(3):701–21.

4. Retamal MA, Froger N, Palacios-Prado N, Ezan P, Saez PJ, Saez JC, et al. Cx43 hemichannels and gap junction channels in astrocytes are regulated oppositely by proinflammatory cytokines released from activated microglia. J Neurosci. 2007;27(50):13781–92.

5. Laird DW. The gap junction proteome and its relationship to disease. Trends Cell Biol. 2010;20(2):92–101.

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