Trophic Factor Withdrawal Induces a Novel Pathway: p38 MAPK Activates NHE1 Resulting in Intracellular Alkalinization, an Early Step in Apoptosis | Zendy

Annette R. Khaled | Zendy; Kyungjae Kim | Zendy; Kathrin Muegge | Zendy; Craig B. Thompson | Zendy; Larry Fliegel | Zendy; Scott K. Durum | Zendy

Open Access

Trophic Factor Withdrawal Induces a Novel Pathway: p38 MAPK Activates NHE1 Resulting in Intracellular Alkalinization, an Early Step in Apoptosis

Author(s) -

Annette R. Khaled,

Kyungjae Kim,

Kathrin Muegge,

Craig B. Thompson,

Larry Fliegel,

Scott K. Durum

Publication year - 2001

Publication title -

the scientific world journal

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.453

H-Index - 93

eISSN - 2356-6140

pISSN - 1537-744X

DOI - 10.1100/tsw.2001.211

Subject(s) - intracellular , mapk/erk pathway , apoptosis , microbiology and biotechnology , p38 mitogen activated protein kinases , chemistry , signal transduction , biology , biochemistry

. The requirement for cytokines in hematopoiesis is partly attributable to a trophic activity, the protection of cells from apoptosis. For example, interleukin-7 (IL-7) protects lymphocyte progenitor cells from apoptotic death during T cell development (1,2). The survival effect of these cytokines has been partly attributed to the Bcl-2 family of proteins (2,3). However, the trophic action of cytokines involves more than the balance of Bcl-2 family members, since overexpression of Bcl-2 does not completely replace the cytokine survival signal (1,4). Hence, the death-inducing signaling pathways triggered early upon cytokine loss are yet to be fully defined.

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