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Cutting edge: IL-4-mediated protection of primary B lymphocytes from apoptosis via Stat6-dependent regulation of glycolytic metabolism.

Cutting edge: IL-4-mediated protection of primary B lymphocytes from apoptosis via Stat6-dependent regulation of glycolytic metabolism. Research Abstract Details 

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  • Cutting edge: IL-4-mediated protection of primary B lymphocytes from apoptosis via Stat6-dependent regulation of glycolytic metabolism. Abstract Text:

    fay j dufortFay J Dufort,blair f bleimanBlair F Bleiman,maria r guminaMaria R Gumina,derek blairDerek Blair,dean j wagnerDean J Wagner,mary f robertsMary F Roberts,yousef abu-amerYousef Abu-Amer,thomas c chilesThomas C Chiles,

    IL-4 prevents the death of naive B lymphocytes through the up-regulation of antiapoptotic proteins such as Bcl-x(L). Despite studies implicating glucose utilization in growth factor-dependent survival of hemopoietic cells, the role of glucose energy metabolism in maintaining B cell viability by IL-4 is unknown. We show that IL-4 triggers glucose uptake, Glut1 expression, and glycolysis in splenic B cells; this is accompanied by increased cellular ATP. Glycolysis inhibition results in apoptosis, even in the presence of IL-4. IL-4-induced glycolysis occurs normally in B cells deficient in insulin receptor substrate-2 or the p85alpha subunit of PI3K and is not affected by pretreatment with PI3K or MAPK pathway inhibitors. Stat6-deficient B cells exhibit impaired IL-4-induced glycolysis. Cell-permeable, constitutively active Stat6 is effective in restoring IL-4-induced glycolysis in Stat6-deficient B cells. Therefore, besides controlling antiapoptotic proteins, IL-4 mediates B cell survival by regulating glucose energy metabolism via a Stat6-dependent pathway.

    Cutting edge: IL-4-mediated protection of primary B lymphocytes from apoptosis via Stat6-dependent regulation of glycolytic metabolism. Publishing Authors By Initials

    fj dufortFJ Dufort,bf bleimanBF Bleiman,mr guminaMR Gumina,d blairD Blair,dj wagnerDJ Wagner,mf robertsMF Roberts,y abu-amerY Abu-Amer,tc chilesTC Chiles,

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    Cutting edge: IL-4-mediated protection of primary B lymphocytes from apoptosis via Stat6-dependent regulation of glycolytic metabolism. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    VOLUME: 179

    Page Numbers: 4953-7

    Journal Abbreviation: J. Immunol.

    ISSN: 0022-1767

    DAY: 15

    MONTH: Oct

    YEAR: 2007

    Cutting edge: IL-4-mediated protection of primary B lymphocytes from apoptosis via Stat6-dependent regulation of glycolytic metabolism. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 2985117

    Cutting edge: IL-4-mediated protection of primary B lymphocytes from apoptosis via Stat6-dependent regulation of glycolytic metabolism. Keywords Mesh Terms:

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    Grant and Affiliation Information for Cutting edge: IL-4-mediated protection of primary B lymphocytes from apoptosis via Stat6-dependent regulation of glycolytic metabolism.

    AFFILIATION: Department of Biology, Boston college, Chestnut Hill, MA 02467, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NIAID

    GRANT: AI60896

    ACRONYM: AI

    MEDLINETA: J Immunol

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