Document Detail

Echovirus 1 infection induces both stress- and growth-activated mitogen-activated protein kinase pathways and regulates the transcription of cellular immediate-early genes.
MedLine Citation:
PMID:  9770423     Owner:  NLM     Status:  MEDLINE    
We have previously shown that echovirus 1 (EV1) infection increases the mRNA levels of cellular immediate-early (IE) genes in host cells. Here we provide further evidence that the induction of junB, c-jun, and c-fos genes is due to active viral macromolecular synthesis rather than to the interaction of EV1 with its receptor, alpha2beta1 integrin. Nuclear run-on transcription assays indicated that differences in mRNA levels in infected and uninfected cells are brought about by regulation at the transcriptional level. EV1 infection induced the phosphorylation of both the stress-related p38 mitogen-activated protein kinase (MAPK) and the growth signal-related ERK1/2 MAPKs. Studies with selective MAPK inhibitors revealed that p38 was the main inducer of junB expression, whereas both MAPK pathways were involved in the induction of c-fos. Activation of AP-1 genes was also observed to occur during infections with other enteroviruses and with Semliki Forest A7(74) virus, suggesting that the phosphorylation of MAPKs and induction of AP-1 gene expression may be important regulators of host cell behavior during viral infections.
P Huttunen; T Hyypiä; P Vihinen; L Nissinen; J Heino
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Virology     Volume:  250     ISSN:  0042-6822     ISO Abbreviation:  Virology     Publication Date:  1998 Oct 
Date Detail:
Created Date:  1998-11-05     Completed Date:  1998-11-05     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0110674     Medline TA:  Virology     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  85-93     Citation Subset:  IM    
Copyright Information:
Copyright 1998 Academic Press.
MediCity Research Laboratory, Department of Virology, Department of Medical Biochemistry, University of Turku, Tykistökatu 6A, Turku, FIN-20520, Finland.
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MeSH Terms
Antiviral Agents / pharmacology
Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors,  metabolism*
Cell Adhesion
Collagen / metabolism
Enterovirus B, Human / genetics*,  physiology
Enzyme Inhibitors / pharmacology
Gene Expression Regulation, Viral / physiology*
Genes, Immediate-Early / genetics*
Isoxazoles / pharmacology
Poliovirus / physiology
Protein Biosynthesis
Proto-Oncogenes / genetics*
RNA, Messenger / analysis
Receptors, Virus / metabolism
Sarcoma, Experimental
Semliki forest virus / physiology
Transcription Factor AP-1 / metabolism
Transcription, Genetic
Tumor Cells, Cultured
Reg. No./Substance:
0/Antiviral Agents; 0/Enzyme Inhibitors; 0/Isoxazoles; 0/RNA, Messenger; 0/Receptors, Virus; 0/Transcription Factor AP-1; 107355-45-3/Win 54954; 9007-34-5/Collagen; EC Protein Kinases

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