TY - JOUR
T1 - Btk function in B cell development and responsee
AU - Satterthwaite, Anne B.
AU - Li, Zuomei
AU - Witte, Owen N.
N1 - Funding Information:
We thank Julia Shimaoka for assistance with manuscript preparation and Purnima Dubey for helpful suggestions. O.N.W. is an Investigator of the Howard Hughes Medical Institute. Work from our laboratory was partially supported by grant CA12800 (Principal Investigator Randy Wall). Z.L. is a Research Fellow of the National Cancer Institute of Canada supported by the Terry Fox Run.
PY - 1998/8
Y1 - 1998/8
N2 - Mutations in Bruton's tyrosine kinase (Btk) result in the B cell immunodeficiencies XLA in humans and Xid in mice. Both the maintenance of peripheral B cell numbers and their response to B cell antigen receptor (BCR) crosslinking depend on Btk. Btk integrates signals from multiple cell surface receptors, including BCR and G-protein coupled receptors. These Btk dependent signals control B cell proliferation and survival by mediating Ca2+ flux, activating JNK and p38 and inducing cell cycle regulatory genes.
AB - Mutations in Bruton's tyrosine kinase (Btk) result in the B cell immunodeficiencies XLA in humans and Xid in mice. Both the maintenance of peripheral B cell numbers and their response to B cell antigen receptor (BCR) crosslinking depend on Btk. Btk integrates signals from multiple cell surface receptors, including BCR and G-protein coupled receptors. These Btk dependent signals control B cell proliferation and survival by mediating Ca2+ flux, activating JNK and p38 and inducing cell cycle regulatory genes.
KW - B cell antigen receptor (BCR)
KW - Bruton's tyrosine kinase (Btk)
KW - Immunodeficiency
KW - Pleckstrin homology (PH) domain
KW - Tyrosine phosphorylation
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U2 - 10.1006/smim.1998.0123
DO - 10.1006/smim.1998.0123
M3 - Article
C2 - 9695187
AN - SCOPUS:0032147181
SN - 1044-5323
VL - 10
SP - 309
EP - 316
JO - Seminars in Immunology
JF - Seminars in Immunology
IS - 4
ER -