Document Detail

Molecular cloning of multiple splicing variants of JIP-1 preferentially expressed in brain.
MedLine Citation:
PMID:  10098834     Owner:  NLM     Status:  MEDLINE    
Stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) is activated by a variety of cellular or environmental stresses. Proper regulation of the SAPK/JNK pathway may be critical for cell survival or death under various conditions. In this study, we report the molecular cloning of novel isoforms of JIP-1, which harbor a putative phosphotyrosine interaction domain and a helix-loop-helix domain, as well as an SH3 homologous region in the C terminus. Northern analysis indicates that transcription variant jip-1 is expressed in brain and kidney and transcription variants jip-2 and jip-3 are specifically expressed in brain. In situ hybridization data showed that the hybridized jip messages were heavily concentrated in adult brain, and were particularly enriched in the cerebral cortex and hippocampus, the brain regions vulnerable to pathological states such as hypoxia-ischemia, epilepsy, and Alzheimer's disease. All the deduced protein products of the jip transcription variants appear to have a similar property in that they inhibit the SAPK/JNK stimulation when overexpressed. Inhibition of SAPK activation by overexpression of the novel isoform JIP-2a resulted in suppression of etoposide-induced cell death in a neuroglioma cell line, N18TG. These findings suggest that JIP may play an important role in regulation of the SAPK pathway that is involved in stress-induced cellular responses.
I J Kim; K W Lee; B Y Park; J K Lee; J Park; I Y Choi; S J Eom; T S Chang; M J Kim; Y I Yeom; S K Chang; Y D Lee; E J Choi; P L Han
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neurochemistry     Volume:  72     ISSN:  0022-3042     ISO Abbreviation:  J. Neurochem.     Publication Date:  1999 Apr 
Date Detail:
Created Date:  1999-04-13     Completed Date:  1999-04-13     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1335-43     Citation Subset:  IM    
Laboratory for Basic Research, Hanhyo Institutes of Technology, Taejon, Korea.
Data Bank Information
Bank Name/Acc. No.:
GENBANK/AF109768;  AF109769;  AF109770;  AF109771;  AF109772;  AF109773;  AF109774
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MeSH Terms
Adaptor Proteins, Signal Transducing*
Alternative Splicing / physiology*
Apoptosis / genetics
Brain / cytology,  enzymology
Brain Chemistry / physiology*
Carrier Proteins / genetics*
Cloning, Molecular
DNA, Complementary / isolation & purification
Gene Expression Regulation, Enzymologic
Gene Library
JNK Mitogen-Activated Protein Kinases*
MAP Kinase Kinase 4
Mice, Inbred BALB C
Mitogen-Activated Protein Kinase Kinases*
Molecular Sequence Data
Neurons / cytology,  enzymology
Protein Kinases / metabolism
Sequence Homology, Amino Acid
Signal Transduction / physiology
Transcription, Genetic / physiology
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Carrier Proteins; 0/DNA, Complementary; 0/Mapk8ip protein, mouse; EC 2.7.-/Protein Kinases; EC Mitogen-Activated Protein Kinases; EC Kinase Kinase 4; EC Protein Kinase Kinases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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