Document Detail


Human c-Jun N-terminal kinase expression and activation in the nervous system.
MedLine Citation:
PMID:  10101227     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Differential expression and localization of c-Jun N-terminal kinases (JNKs) in the human brain may reflect transduction of a variety of extracellular stimuli to selective cellular responses. Of the three JNKs, JNK1 and 2 are widely distributed in tissues and JNK3 is predominantly restricted to brain where it is expressed in neurons. Although there is considerable molecular conservation among all three JNKs, we distinguished expression of each by in situ hybridization, immunoblot analysis with a panel of antibodies, and stress-activation using c-Jun as substrate. In the human central nervous system (CNS), there are at least 10 isoforms: JNK3alpha1 and JNK1alpha1 were the major JNK isoforms expressed; JNK2 was not detected. On immunoblots of brain homogenates, antibody selectivity identified JNK3alpha1 as a 45-kDa protein, JNK1alpha1, a slightly lower band at 44 kDa, and a 50-kDa band of unknown specificity. Recombinant human JNK3alpha1, transfected either into CHO, COS-1, or Neuro2A (N2A) cells, was strongly expressed as a 45-kDa protein in each. Transfected JNK3alpha1, and endogenous JNK1, each immunoprecipitated from N2A cells, phosphorylated recombinant forms of human c-Jun. Kinase activity of each JNK was modestly stimulated in N2A cells by anisomycin but not by ceramide, UV irradiation, or heat shock. Endogenous JNK activation, especially at a low level, may reflect a chronic and cumulative stress process that contributes to hyperphosphorylation of cytoskeletal proteins such as those found in Alzheimer's disease (AD), and ultimately, induction of apoptosis.
Authors:
Y Kumagae; Y Zhang; O J Kim; C A Miller
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Brain research. Molecular brain research     Volume:  67     ISSN:  0169-328X     ISO Abbreviation:  Brain Res. Mol. Brain Res.     Publication Date:  1999 Apr 
Date Detail:
Created Date:  1999-05-21     Completed Date:  1999-05-21     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8908640     Medline TA:  Brain Res Mol Brain Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  10-7     Citation Subset:  IM    
Copyright Information:
Copyright 1999 Published by Elsevier Science B.V.
Affiliation:
Neuroscience Research Laboratories, Sankyo, Shinagawa-ku, Tokyo 140, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibody Specificity
Calcium-Calmodulin-Dependent Protein Kinases / analysis,  genetics*,  immunology
Gene Expression Regulation, Enzymologic
Gene Expression Regulation, Neoplastic
Hippocampus / chemistry,  cytology,  enzymology*
Humans
In Situ Hybridization
JNK Mitogen-Activated Protein Kinases
Mice
Mitogen-Activated Protein Kinase 10
Mitogen-Activated Protein Kinase 9
Mitogen-Activated Protein Kinases*
Neuroblastoma
Neurons / chemistry,  enzymology
Phosphorylation
Precipitin Tests
Protein Kinases / analysis,  genetics,  immunology
Protein-Serine-Threonine Kinases / metabolism
Protein-Tyrosine Kinases / metabolism
Proto-Oncogene Proteins c-jun / metabolism
RNA, Messenger / analysis
Recombinant Proteins / analysis,  genetics,  immunology
Stress, Physiological / metabolism
Transfection
Tumor Cells, Cultured / enzymology
tau Proteins / metabolism
Grant Support
ID/Acronym/Agency:
5R37-MH39145/MH/NIMH NIH HHS; P50-AG05142/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/Proto-Oncogene Proteins c-jun; 0/RNA, Messenger; 0/Recombinant Proteins; 0/tau Proteins; EC 2.7.-/Protein Kinases; EC 2.7.1.-/Mitogen-Activated Protein Kinase 10; EC 2.7.1.24/Mitogen-Activated Protein Kinase 9; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.17/Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.24/JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24/Mitogen-Activated Protein Kinases

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