Title |
ATP11C is critical for the internalization of phosphatidylserine and differentiation of B lymphocytes
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Published in |
Nature Immunology, March 2011
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DOI | 10.1038/ni.2011 |
Pubmed ID | |
Authors |
Mehmet Yabas, Charis E Teh, Sandra Frankenreiter, Dennis Lal, Carla M Roots, Belinda Whittle, Daniel T Andrews, Yafei Zhang, Narci C Teoh, Jonathan Sprent, Lina E Tze, Edyta M Kucharska, Jennifer Kofler, Geoffrey C Farell, Stefan Bröer, Christopher C Goodnow, Anselm Enders |
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. |
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Demographic breakdown
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Researcher | 21 | 18% |
Student > Master | 14 | 12% |
Professor | 9 | 8% |
Professor > Associate Professor | 9 | 8% |
Other | 18 | 15% |
Unknown | 22 | 19% |
Readers by discipline | Count | As % |
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Immunology and Microbiology | 6 | 5% |
Neuroscience | 3 | 3% |
Other | 5 | 4% |
Unknown | 23 | 20% |