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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2011-4-19
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pubmed:abstractText |
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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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
1529-2916
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pubmed:author |
pubmed-author:AndrewsDaniel TDT,
pubmed-author:BröerStefanS,
pubmed-author:EndersAnselmA,
pubmed-author:FarellGeoffrey CGC,
pubmed-author:FrankenreiterSandraS,
pubmed-author:GoodnowChristopher CCC,
pubmed-author:KoflerJenniferJ,
pubmed-author:KucharskaEdyta MEM,
pubmed-author:LalDennisD,
pubmed-author:RootsCarla MCM,
pubmed-author:SprentJonathanJ,
pubmed-author:TehCharis ECE,
pubmed-author:TeohNarci CNC,
pubmed-author:TzeLina ELE,
pubmed-author:WhittleBelindaB,
pubmed-author:YabasMehmetM,
pubmed-author:ZhangYafeiY
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pubmed:issnType |
Electronic
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
441-9
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pubmed:dateRevised |
2011-11-8
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pubmed:meshHeading |
pubmed-meshheading:21423173-Adenosine Triphosphatases,
pubmed-meshheading:21423173-Animals,
pubmed-meshheading:21423173-B-Lymphocytes,
pubmed-meshheading:21423173-Base Sequence,
pubmed-meshheading:21423173-Cell Differentiation,
pubmed-meshheading:21423173-Endocytosis,
pubmed-meshheading:21423173-Female,
pubmed-meshheading:21423173-Flow Cytometry,
pubmed-meshheading:21423173-Genes, bcl-2,
pubmed-meshheading:21423173-Interleukin-7,
pubmed-meshheading:21423173-Liver,
pubmed-meshheading:21423173-Male,
pubmed-meshheading:21423173-Mice,
pubmed-meshheading:21423173-Mice, Inbred C57BL,
pubmed-meshheading:21423173-Mice, Inbred CBA,
pubmed-meshheading:21423173-Mice, Knockout,
pubmed-meshheading:21423173-Mice, Transgenic,
pubmed-meshheading:21423173-Molecular Sequence Data,
pubmed-meshheading:21423173-Mutagenesis,
pubmed-meshheading:21423173-Phosphoserine,
pubmed-meshheading:21423173-RNA, Messenger,
pubmed-meshheading:21423173-Reverse Transcriptase Polymerase Chain Reaction
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pubmed:year |
2011
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pubmed:articleTitle |
ATP11C is critical for the internalization of phosphatidylserine and differentiation of B lymphocytes.
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pubmed:affiliation |
Ramaciotti Immunization Genomics Laboratory, Department of Immunology, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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