Essential, Nonredundant Role for the Phosphoinositide 3-Kinase p110δ in Signaling by the B-Cell Receptor Complex-Reference-Cited by-同舟云学术

Essential, Nonredundant Role for the Phosphoinositide 3-Kinase p110δ in Signaling by the B-Cell Receptor Complex

Published:2002-12-15 Issue:24 Volume:22 Page:8580-8591
ISSN:0270-7306
Container-title:Molecular and Cellular Biology
language:en
Short-container-title:Mol Cell Biol

Author:

Jou Shiann-Tarng¹,Carpino Nick¹,Takahashi Yutaka¹,Piekorz Roland²¹,Chao Jyh-Rong¹,Carpino Neena¹,Wang Demin¹,Ihle James N.²¹³

Affiliation:

1. Department of Biochemistry, St. Jude Children's Research Hospital, Memphis, Tennessee 38105

2. Howard Hughes Medical Institute

3. Department of Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee 38063

Abstract

ABSTRACT Many receptor and nonreceptor tyrosine kinases activate phosphoinositide 3-kinases (PI3Ks). To assess the role of the δ isoform of the p110 catalytic subunit of PI3Ks, we derived enzyme-deficient mice. The mice are viable but have decreased numbers of mature B cells, a block in pro-B-cell differentiation, and a B1 B-cell deficiency. Both immunoglobulin M receptor-induced Ca 2+ flux and proliferation in response to B-cell mitogens are attenuated. Immunoglobulin levels are decreased substantially. The ability to respond to T-cell-independent antigens is markedly reduced, and the ability to respond to T-cell-dependent antigens is completely eliminated. Germinal center formation in the spleen in response to antigen stimulation is disrupted. These results define a nonredundant signaling pathway(s) utilizing the δ isoform of p110 PI3K for the development and function of B cells.

Publisher

American Society for Microbiology

Subject

Cell Biology,Molecular Biology

Link

https://journals.asm.org/doi/pdf/10.1128/MCB.22.24.8580-8591.2002

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