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Article
Cited 84 time in webofscience Cited 83 time in scopus
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Authors
Yabas, MTeh, CEFrankenreiter, SLal, DCarla M RootscloseBelinda WhittleDaniel T AndrewsYafei ZhangNarci C Teoh,Sprent, JLina E TzeEdyta M KucharskaJennifer Kofler,Geoffrey C FarellStefan BröerChristopher C Goodnow2, 7Anselm Enders1, 7
Date Issued
Feb-2011
Publisher
NATURE IMMUNOLOGY
Abstract
Subcompartments of the plasma membrane are believed to be critical for lymphocyte responses, but few genetic tools are available to test their function. Here we describe a previously unknown X-linked B cell-deficiency syndrome in mice caused by mutations in Atp11c, which encodes a member of the P4 ATPase family thought to serve as 'flippases' that concentrate aminophospholipids in the cytoplasmic leaflet of cell membranes. Defective ATP11C resulted in a lower rate of phosphatidylserine translocation in pro-B cells and much lower pre-B cell and B cell numbers despite expression of pre-rearranged immunoglobulin transgenes or enforced expression of the prosurvival protein Bcl-2 to prevent apoptosis and abolished pre-B cell population expansion in response to a transgene encoding interleukin 7. The only other abnormalities we noted were anemia, hyperbilirubinemia and hepatocellular carcinoma. Our results identify an intimate connection between phospholipid transport and B lymphocyte function.
URI
http://oasis.postech.ac.kr/handle/2014.oak/17288
DOI
10.1038/NI.2011
ISSN
1529-2908
Article Type
Article
Citation
NATURE IMMUNOLOGY, vol. 12, no. 5, page. 441 - U100, 2011-02
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