Journal
NATURE IMMUNOLOGY
Volume 4, Issue 3, Pages 274-279Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni893
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Funding
- NHLBI NIH HHS [HL54476] Funding Source: Medline
- NIAID NIH HHS [AI053545-01] Funding Source: Medline
- NIDDK NIH HHS [DK58066] Funding Source: Medline
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The nature of signals that govern the development of immunoglobulin heavy chain-dependent B cells is largely unknown. Using mice deficient for the B cell-expressed Src-family protein tyrosine kinases (SFKs) Blk, Fyn and Lyn, we show an essential role of these kinases in pre-B cell receptor (pre-BCR)-mediated NF-kappaB activation and B cell development. This signaling defect is SFK specific, as a deficiency in Syk, which controls pre-B cell development, does not affect NF-kappaB induction. Impaired NF-kappaB induction was overcome by the activation of protein kinase C (PKC)-lambda, thus suggesting the involvement of PKC-lambda in pre-BCR-mediated SFK-dependent activation of NF-kappaB. Our data show the existence of a functionally distinct SFK signaling module responsible for pre-BCR-mediated NF-kappaB activation and B cell development.
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