CD22 attenuates calcium signaling by potentiating plasma membrane calcium-ATPase activity

被引：0
作者：
Jie Chen
Paul A McLean
Benjamin G Neel
Gbolahan Okunade
Gary E Shull
Henry H Wortis
机构：
[1] Tufts University School of Medicine and Graduate Program in Genetics,Department of Pathology
[2] Sackler School of Graduate Biomedical Sciences,Division of Hematology
[3] Cancer Biology Program,Oncology, Department of Medicine
[4] Beth Israel Deaconess Medical Center,Department of Molecular Genetics
[5] Harvard Medical School,undefined
[6] Biochemistry and Microbiology,undefined
[7] The University of Cincinnati College of Medicine,undefined
[8] Point Therapeutics,undefined
来源：
Nature Immunology | 2004年 / 5卷
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摘要：
Binding of antigen to the B cell receptor induces a calcium response, which is required for proliferation and antibody production. CD22, a B cell surface protein, inhibits this signal through mechanisms that have been obscure. We report here that CD22 augments calcium efflux after B cell receptor crosslinking. Inhibition of plasma membrane calcium-ATPase (PMCA) attenuated these effects, as did disruption by homologous recombination of the gene encoding PMCA4a and PMCA4b. PMCA coimmunoprecipitated with CD22 in an activation-dependent way. CD22 cytoplasmic tyrosine residues were required for association with PMCA and enhancement of calcium efflux. Moreover, CD22 regulation of efflux and the calcium response required the tyrosine phosphatase SHP-1. Thus, SHP-1 and PMCA provide a mechanism by which CD22, a tissue-specific negative regulator, can affect calcium responses.
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页码：651 / 657
页数：6
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