Document Detail


Expression of c-fos, c-jun, and c-jun N-terminal kinase (JNK) in a developmental model of induced apoptotic death in neurons of the substantia nigra.
MedLine Citation:
PMID:  9930727     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The transcription factors c-fos and c-jun have been proposed to play a role in the initiation of programmed cell death in neurons. We have shown that programmed cell death, with the morphology of apoptosis, occurs in dopamine neurons of the substantia nigra (SN) during normal postnatal development and that this death event can be induced by early striatal target injury. We have investigated the relationship between c-fos and c-jun protein expression and induced death in neurons of the SN. Although c-fos is induced, it is unlikely to play a role in cell death, because its expression is not well correlated with apoptotic death either temporally or at a cellular level. Expression of c-jun, however, is both temporally and regionally correlated with induction of death, and, at a cellular level, it colocalizes with apoptotic morphology. The increased expression of c-jun is likely to be functionally significant, because it is associated with increased c-jun N-terminal kinase (JNK) and phosphorylated c-jun expression. JNK expression also colocalizes with apoptotic morphology. We conclude that c-jun is likely to play a role in the initiation of apoptotic cell death in these neurons.
Authors:
T F Oo; C Henchcliffe; D James; R E Burke
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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:  Journal of neurochemistry     Volume:  72     ISSN:  0022-3042     ISO Abbreviation:  J. Neurochem.     Publication Date:  1999 Feb 
Date Detail:
Created Date:  1999-02-11     Completed Date:  1999-02-11     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  557-64     Citation Subset:  IM    
Affiliation:
Department of Neurology, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology*
Dopamine / physiology
Female
JNK Mitogen-Activated Protein Kinases*
MAP Kinase Kinase 4
Mitogen-Activated Protein Kinase Kinases*
Nerve Degeneration / chemically induced
Neurons / cytology,  enzymology*
Neurotoxins / pharmacology
Parkinson Disease / metabolism
Pregnancy
Protein Kinases / biosynthesis*
Proto-Oncogene Proteins c-fos / biosynthesis*
Proto-Oncogene Proteins c-jun / biosynthesis*
Quinolinic Acid
Rats
Substantia Nigra / cytology,  embryology
Grant Support
ID/Acronym/Agency:
NS 26836/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Neurotoxins; 0/Proto-Oncogene Proteins c-fos; 0/Proto-Oncogene Proteins c-jun; 89-00-9/Quinolinic Acid; EC 2.7.-/Protein Kinases; EC 2.7.11.24/JNK Mitogen-Activated Protein Kinases; EC 2.7.12.2/MAP Kinase Kinase 4; EC 2.7.12.2/Mitogen-Activated Protein Kinase Kinases

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


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