دورية أكاديمية

Cross-talk between JIP3 and JIP1 during glucose deprivation: SEK1-JNK2 and Akt1 act as mediators.

التفاصيل البيبلوغرافية
العنوان: Cross-talk between JIP3 and JIP1 during glucose deprivation: SEK1-JNK2 and Akt1 act as mediators.
المؤلفون: Song JJ; Department of Surgery and Pharmacology, University of Pittsburgh, Pittsburgh, Pennsylvania 15213, USA., Lee YJ
المصدر: The Journal of biological chemistry [J Biol Chem] 2005 Jul 22; Vol. 280 (29), pp. 26845-55. Date of Electronic Publication: 2005 May 23.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
اللغة: English
بيانات الدورية: Publisher: Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology Country of Publication: United States NLM ID: 2985121R Publication Model: Print-Electronic Cited Medium: Print ISSN: 0021-9258 (Print) Linking ISSN: 00219258 NLM ISO Abbreviation: J Biol Chem Subsets: MEDLINE
أسماء مطبوعة: Publication: 2021- : [New York, NY] : Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology
Original Publication: Baltimore, MD : American Society for Biochemistry and Molecular Biology
مواضيع طبية MeSH: Adaptor Proteins, Signal Transducing/*metabolism , Glucose/*deficiency , MAP Kinase Kinase 4/*metabolism , Mitogen-Activated Protein Kinase 9/*metabolism , Nerve Tissue Proteins/*metabolism , Protein Serine-Threonine Kinases/*metabolism , Proto-Oncogene Proteins/*metabolism, Cell Line, Tumor ; Humans ; MAP Kinase Kinase Kinase 5/metabolism ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; Receptor Cross-Talk ; Signal Transduction
مستخلص: 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.
معلومات مُعتمدة: CA95191 United States CA NCI NIH HHS; CA96989 United States CA NCI NIH HHS
المشرفين على المادة: 0 (Adaptor Proteins, Signal Transducing)
0 (MAPK8IP1 protein, human)
0 (MAPK8IP3 protein, human)
0 (Nerve Tissue Proteins)
0 (Proto-Oncogene Proteins)
EC 2.7.1.24 (Mitogen-Activated Protein Kinase 9)
EC 2.7.11.1 (AKT1 protein, human)
EC 2.7.11.1 (Protein Serine-Threonine Kinases)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
EC 2.7.11.25 (MAP Kinase Kinase Kinase 5)
EC 2.7.12.2 (MAP Kinase Kinase 4)
IY9XDZ35W2 (Glucose)
تواريخ الأحداث: Date Created: 20050525 Date Completed: 20050909 Latest Revision: 20211203
رمز التحديث: 20240829
DOI: 10.1074/jbc.M502318200
PMID: 15911620
قاعدة البيانات: MEDLINE
الوصف
تدمد:0021-9258
DOI:10.1074/jbc.M502318200