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Cross-talk between JIP3 and JIP1 during Glucose Deprivation: SEK1-JNK2 and Akt1 act as mediators

Authors
 Jae J. Song  ;  Yong J. Lee 
Citation
 JOURNAL OF BIOLOGICAL CHEMISTRY, Vol.280(29) : 26845-26855, 2005 
Journal Title
 JOURNAL OF BIOLOGICAL CHEMISTRY 
ISSN
 0021-9258 
Issue Date
2005
MeSH
Adaptor Proteins, Signal Transducing/metabolism* ; Cell Line, Tumor ; Glucose/deficiency* ; Humans ; MAP Kinase Kinase 4/metabolism* ; MAP Kinase Kinase Kinase 5/metabolism ; Mitogen-Activated Protein Kinase 9/metabolism* ; Nerve Tissue Proteins/metabolism* ; Phosphorylation ; Protein-Serine-Threonine Kinases/metabolism* ; Proto-Oncogene Proteins/metabolism* ; Proto-Oncogene Proteins c-akt ; Receptor Cross-Talk ; Signal Transduction
Keywords
15911620
Abstract
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 that 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.
Files in This Item:
T200504612.pdf Download
DOI
10.1074/jbc.M502318200
Appears in Collections:
5. Research Institutes (연구소) > Institute for Cancer Research (암연구소) > 1. Journal Papers
Yonsei Authors
Song, Jae Jin(송재진) ORCID logo https://orcid.org/0000-0001-8183-9550
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/114962
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