期刊
NATURE IMMUNOLOGY
卷 12, 期 5, 页码 441-U100出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2011
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资金
- National Institutes of Health
- Wellcome Trust
- Australian Research Council
- National Health and Medical Research Council
- Ramaciotti Foundation
- Ministry of National Education, Republic of Turkey
- Deutsche Forschungsgemeinschaft [EN 790/1-1]
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.
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