Stress-activated Protein Kinases: Activation, Regulation and Function

Paul, Andrew; Wilson, Susan L.; Belham, Christopher; Robinson, Caspar J. M.; Scott, Pamela Sharkey; Gould, Gwyn W.; Plevin, Robin

doi:10.1016/s0898-6568(97)00042-9

Cited by 293 publications

(206 citation statements)

References 91 publications

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“…2). TNF receptors conduct many of their cellular effects through the activation of the ERK families MAPK, p38 MAPK, and JNK (18), as well as the NF-B transcription factor (19). Because p38 MAPK and JNK stress kinases have been described as proapoptotic (8,20,21), we ascertained the ability of TNF to evoke p38 MAPK, JNK, and MAPK activity in life and death TF-1 phenotypes (Fig.…”

Section: Sds͞page and Westernmentioning

confidence: 99%

Switching leukemia cell phenotype between life and death

Tucker

Rae

Littlejohn³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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Section: Sds͞page and Westernmentioning

confidence: 99%

Switching leukemia cell phenotype between life and death

Tucker

Rae

Littlejohn³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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“…AP-1 transcriptional activity is stimulated by JNK phosphorylation of c-jun, a component of AP-1 (reviewed by Karin, 1995;Paul et al, 1997).…”

Section: Responses Mediated By Jnk and C-ablmentioning

confidence: 99%

ATM: A mediator of multiple responses to genotoxic stress

1999

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The ATM protein kinase is the product of the gene responsible for the pleiotropic recessive disorder ataxiatelangiectasia. ATM-de®cient cells show enhanced sensitivity and greatly reduced responses to genotoxic agents that generate DNA double strand breaks (DSBs), such as ionizing radiation and radiomimetic chemicals, but exhibit normal responses to DNA adducts and base modi®cations induced by other agents. Therefore, DSBs are most likely the predominant signal for the activation of ATM-mediated pathways. Identi®cation of the ATM gene triggered extensive research aimed at elucidating the numerous functions of its large multifaceted protein product. While ATM has both nuclear and cytoplasmic functions, this review will focus on its roles in the nucleus where it plays a central role in the very early stages of damage detection and serves as a master controller of cellular responses to DSBs. By activating key regulators of multiple signal transduction pathways, ATM mediates the e cient induction of a signaling network responsible for repair of the damage, and for cellular recovery and survival.

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“…The other two MAPK members, SAPK/JNK and p38/mHOG, are involved in stress-induced signaling mechanisms. The most potent activators of these kinases are most notably cytokines such as interleukin-1b (IL1b), tumor necrosis factor-a (TNF-a), and ultraviolet (UV) irradiation (Geng et al, 1996;Kyriakis and Avruch, 1996;Zanke et al, 1996a, b;Paul et al, 1997). These MAPKs are activated by phosphorylation on specific tyrosine and threonine residues by upstream dual kinases referred to as MAPK kinases (or MKKs).…”

Section: Introductionmentioning

confidence: 99%