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10.1016/j.celrep.2018.06.035 http://scihub22266oqcxt.onion/10.1016/j.celrep.2018.06.035 C6057491!6057491!29996100     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Rep 2018 ; 24 (2): 391-405 Nephropedia Template TP {{tp|p=29996100|t=2018. PI3K-Mediated Blimp-1 Activation Controls B Cell Selection and Homeostasis |pdf=|usr=}}{{29996100}} gab.com Text PI3K-Mediated Blimp-1 Activation Controls B Cell Selection and Homeostasis JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=29996100 #FOAvip Activation of phosphoinositide 3-kinase (PI3K) signaling plays a central role in regulating proliferation and survival of B cells. Here, we tested the hypothesis that B cell receptor (BCR)-mediated activation of PI3K induces the terminal differentiation factor Blimp-1 that interferes with proliferation and survival, thereby controlling the expansion of activated B cells. In fact, B-cell-specific inactivation of Pten, the negative regulator of PI3K signaling, leads to deregulated PI3K activity and elevated Blimp-1 expression. Combined deficiency for Pten and Blimp-1 results in abnormal expansion of B-1 B cells and splenomegaly. Interestingly, Blimp-1 also acts at early stages of B cell development to regulate B cell selection, as Blimp-1 deficiency results in an increased proportion of autoreactive B cells. Together, our data suggest that the combined requirement of deregulated PI3K signaling in addition to defective terminal differentiation represents the basis for proper selection and expansion of developing B cells. Twit Text FOAVip PI3K-Mediated Blimp-1 Activation Controls B Cell Selection and Homeostasis ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=29996100 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29996100 #FOAvip English Wikipedia <ref>{{Cite pmid|29996100}}</ref> PI3K-Mediated Blimp-1 Activation Controls B Cell Selection and Homeostasis #MMPMID29996100 Setz CS; Hug E; Khadour A; Abdelrasoul H; Bilal M; Hobeika E; Jumaa H Cell Rep 2018[Jul]; 24 (2): 391-405 PMID29996100show ga Activation of phosphoinositide 3-kinase (PI3K) signaling plays a central role in regulating proliferation and survival of B cells. Here, we tested the hypothesis that B cell receptor (BCR)-mediated activation of PI3K induces the terminal differentiation factor Blimp-1 that interferes with proliferation and survival, thereby controlling the expansion of activated B cells. In fact, B-cell-specific inactivation of Pten, the negative regulator of PI3K signaling, leads to deregulated PI3K activity and elevated Blimp-1 expression. Combined deficiency for Pten and Blimp-1 results in abnormal expansion of B-1 B cells and splenomegaly. Interestingly, Blimp-1 also acts at early stages of B cell development to regulate B cell selection, as Blimp-1 deficiency results in an increased proportion of autoreactive B cells. Together, our data suggest that the combined requirement of deregulated PI3K signaling in addition to defective terminal differentiation represents the basis for proper selection and expansion of developing B cells. äPI3K-Mediated Blimp-1 Activation Controls B Cell Selection and Homeost(epmc).pdf DeepDyve Pubget Overpricing