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Signaling pathway to BCR-induced Mcl-1 expression.

By Mary Kaileh (846540), Estefania Vazquez (846541), Alexander W. MacFarlane IV (846542), Kerry Campbell (846543), Tomohiro Kurosaki (846544), Ulrich Siebenlist (462174) and Ranjan Sen (218595)


<p>(A, B) CD43<sup>-</sup> splenic B cells from Bim<sup>-/-</sup> mice were treated with anti-IgM F(ab’)<sub>2</sub> (15μg/ml) for various times in the presence or absence of Syk kinase inhibitor R406 (4μM), Bruton’s tyrosine kinase inhibitor Ibrutinib (PCI-32765) (20nM), or TORC1 inhibitor rapamycin (50nM). Whole cell extracts were fractionated by SDS-PAGE and Mcl-1 protein was analyzed by immunoblotting. β-actin was used as a loading control to normalize between samples. (C, D) CD43<sup>-</sup> splenic B cells from BL6, BCAP<sup>-/-</sup> (C) or CD19<sup>-/-</sup> (D) mice were cultured for the indicated times with or without anti-IgM F(ab’)<sub>2</sub> (15μg/ml). Whole cell extracts were prepared and assayed for Mcl-1 levels by Western blot analysis. β-actin was used as a loading control to normalize between samples. Representative gels from 3 independent experiments are shown for A and B and 2 independent experiments for C and D. Cell viability profile of BCAP<sup>-/-</sup> and CD19<sup>-/-</sup> B cells are shown in <a href="" target="_blank">S4 Fig</a>.</p

Topics: Biological Sciences, b cells, Independent Survival Signaling, B Lymphocytes Peripheral B lymphocyte survival, p 100 expression, bcr, signal, B cell receptor, baff, pathways increase Mcl, PI 3K pathway, B Cell Survival
Year: 2016
DOI identifier: 10.1371/journal.pone.0146955.g002
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Provided by: FigShare
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