PI3K and Btk differentially regulate B cell antigen receptor-mediated signal transduction. Export

@article{citeulike:6029028, abstract = {Phosphoinositide-3 kinase (PI3K) is thought to activate the tyrosine kinase Btk. However, through analysis of PI3K-/- and Btk-/- mice, B cell antigen receptor (BCR)-induced activation of Btk in mouse B cells was found to be unaffected by PI3K inhibitors or by a lack of PI3K. Consistent with this observation, PI3K-/- Btk-/- double-deficient mice had more severe defects than either single-mutant mouse. NF-kappaB activation along with Bcl-xL and cyclin D2 induction were severely blocked in both PI3K-/- and Btk-/- single-deficient B cells. Transgenic expression of Bcl-xL restored the development and BCR-induced proliferation of B cells in PI3K-/- mice. Our results indicate that PI3K and Btk have unique roles in proximal BCR signaling and that they have a common target further downstream in the activation of NF-kappaB.}, author = {Suzuki, Harumi and Matsuda, Satoshi and Terauchi, Yasuo and Fujiwara, Mari and Ohteki, Toshiaki and Asano, Tomoichiro and Behrens, Timothy W. and Kouro, Taku and Takatsu, Kiyoshi and Kadowaki, Takashi and Koyasu, Shigeo}, citeulike-article-id = {6029028}, citeulike-linkout-0 = {http://dx.doi.org/10.1038/ni890}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/12563258}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=12563258}, doi = {10.1038/ni890}, issn = {1529-2908}, journal = {Nature immunology}, keywords = {bcr, btk, pi3k}, month = {March}, number = {3}, pages = {280--286}, posted-at = {2009-10-28 21:47:18}, priority = {2}, title = {PI3K and Btk differentially regulate B cell antigen receptor-mediated signal transduction.}, url = {http://dx.doi.org/10.1038/ni890}, volume = {4}, year = {2003} }

TY - JOUR ID - citeulike:6029028 L3 - citeulike-article-id:6029028 N2 - Phosphoinositide-3 kinase (PI3K) is thought to activate the tyrosine kinase Btk. However, through analysis of PI3K-/- and Btk-/- mice, B cell antigen receptor (BCR)-induced activation of Btk in mouse B cells was found to be unaffected by PI3K inhibitors or by a lack of PI3K. Consistent with this observation, PI3K-/- Btk-/- double-deficient mice had more severe defects than either single-mutant mouse. NF-kappaB activation along with Bcl-xL and cyclin D2 induction were severely blocked in both PI3K-/- and Btk-/- single-deficient B cells. Transgenic expression of Bcl-xL restored the development and BCR-induced proliferation of B cells in PI3K-/- mice. Our results indicate that PI3K and Btk have unique roles in proximal BCR signaling and that they have a common target further downstream in the activation of NF-kappaB. IS - 3 JF - Nature immunology SN - 1529-2908 EP - 286 TI - PI3K and Btk differentially regulate B cell antigen receptor-mediated signal transduction. VL - 4 SP - 280 KW - bcr KW - btk KW - pi3k AU - Suzuki, Harumi AU - Matsuda, Satoshi AU - Terauchi, Yasuo AU - Fujiwara, Mari AU - Ohteki, Toshiaki AU - Asano, Tomoichiro AU - Behrens, Timothy AU - Kouro, Taku AU - Takatsu, Kiyoshi AU - Kadowaki, Takashi AU - Koyasu, Shigeo PY - 2003/03// UR - http://dx.doi.org/10.1038/ni890 ER -