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Carcinogenesis 7: Inflammation, Reactive Oxygen Species, and Cancer

Cross-talk between JIP3 and JIP1 during metabolic oxidative stress: SEK1-JNK2 and Akt1 act as mediators

Yong J. Lee and Jae J. Song
Yong J. Lee
University of Pittsburgh, Pittsburgh, PA
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Jae J. Song
University of Pittsburgh, Pittsburgh, PA
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DOI:  Published April 2006
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Proc Amer Assoc Cancer Res, Volume 47, 2006

Abstract

3550

We have previously observed that glucose deprivation activates the ASK1-MEK-MAPK signal transduction pathway. In the present study, we reveal that two scaffolding proteins, JIP1 and JIP3, have a cross-talk which leads to the regulation of the ASK1-SEK1-JNK signal during glucose deprivation. Glucose deprivation rapidly increases the interaction between ASK1 and JIP3 and the consequently activated ASK1 phosphorylates SEK1 on the Thr-261 residue. The activated SEK1 dissociates from JIP3 and phosphorylates JNK2 on the Tyr-185 residue. Phosphorylated JNK2 binds to JIP1 and the phosphorylation of the Thr-183 residue of JNK2 occurs. JNK2 phosphorylates JIP1 on the Thr-103 residue and leads to dissociation of Akt1 from JIP1. Dissociated Akt1 binds to SEK1 and ASK1, and inhibits their enzyme activity by phosphorylating SEK1 on the Ser-80 residue and ASK1 on the Ser-83 residue. Taken together, our data demonstrate that cross-talk between JIP3 and JIP1 is mediated through SEK1-JNK2 and Akt1.

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Cancer Research: 66 (8 Supplement)
April 2006
Volume 66, Issue 8 Supplement
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Cross-talk between JIP3 and JIP1 during metabolic oxidative stress: SEK1-JNK2 and Akt1 act as mediators
Yong J. Lee and Jae J. Song
Cancer Res April 15 2006 (66) (8 Supplement) 833;

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Cross-talk between JIP3 and JIP1 during metabolic oxidative stress: SEK1-JNK2 and Akt1 act as mediators
Yong J. Lee and Jae J. Song
Cancer Res April 15 2006 (66) (8 Supplement) 833;
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Show more Carcinogenesis 7: Inflammation, Reactive Oxygen Species, and Cancer
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Cancer Research Online ISSN: 1538-7445
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