Elucidation of physiological function of store-operated calcium influx in B cells and its molecular mechanism.
Project/Area Number |
21790469
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Immunology
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Research Institution | Osaka University |
Principal Investigator |
BABA Yoshihiro Osaka University, 免疫学フロンティア研究センター, 特任准教授 (20415269)
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Project Period (FY) |
2009 – 2010
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Project Status |
Completed (Fiscal Year 2010)
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Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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Keywords | B細胞 / ストア作動性カルシウム流入 / STIM1 / STIM2 |
Research Abstract |
We established Stim2-deficient DT40 B cells and analyzed the functional difference between STIM1 and STIM2. We generated Stim2-deficient mice, but these are lethal about 4~5 weeks after birth. Furthermore, we found that B cells lacking STIM1 and STIM2 were defective in BCR-evoked NFAT activation and IL-10 production, suggesting that STIM proteins are essential for suppressive function through NFAT-dependent IL-10.
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Report
(3 results)
Research Products
(19 results)
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[Journal Article] S-glutathionylation activates STIM1 and alters mitochondrial homeostasis.2010
Author(s)
Hawkins BJ, Irrinki KM, Mallilankaraman K, Lien YC, Wang Y, Bhanumathy CD, Subbiah R, Ritchie MF, Soboloff J, Baba Y, Kurosaki T, Joseph SK, Gill DL, Madesh M.
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Journal Title
J.Cell Biol. 190
Pages: 391-405
Related Report
Peer Reviewed
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