Document Detail


Delay in serum stimulation of Erk activity caused by oncogenic transformation.
MedLine Citation:
PMID:  8622889     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Mitogenic growth factor stimulation activates several signal transduction pathways, including the well-characterized Ras-Erk pathway, resulting in transient activation of Erk1 and Erk2. Oncogenic transformation, however, causes constitutive activation of growth signalling pathways, resulting in an accelerated rate of cell division. We investigated the effects of transformation on serum and growth factor stimulation of Erk1 and Erk2, and show that stimulation of these MAP kinases, as well as the Erk activator Mek, is delayed in oncogene transformed cells. Possible mechanisms of this delay are explored. In addition, our data indicate that prolonged mitogenic stimulation does not necessarily result in constitutive activation of Erk1 and Erk2.
Authors:
H Greulich; C Reichman; H Hanafusa
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Oncogene     Volume:  12     ISSN:  0950-9232     ISO Abbreviation:  Oncogene     Publication Date:  1996 Apr 
Date Detail:
Created Date:  1996-06-18     Completed Date:  1996-06-18     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8711562     Medline TA:  Oncogene     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  1689-95     Citation Subset:  IM    
Affiliation:
Laboratory of Molecular Oncology, Rockefeller University, New York, NY 10021, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Calcium-Calmodulin-Dependent Protein Kinases / drug effects,  genetics,  metabolism*
Cell Cycle Proteins*
Cell Line, Transformed
Cell Transformation, Neoplastic*
Chick Embryo
Culture Media, Serum-Free
Dual Specificity Phosphatase 1
Enzyme Activation / drug effects,  genetics*
Fibroblasts
Genes, ras
Immediate-Early Proteins / genetics,  metabolism
Mitogen-Activated Protein Kinase 1
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinase Kinases
Mitogen-Activated Protein Kinases*
Mutation
Oncogene Protein v-crk
Phosphoprotein Phosphatases*
Phosphorylation
Protein Kinases / metabolism
Protein Phosphatase 1
Protein Tyrosine Phosphatases / genetics,  metabolism
Protein-Tyrosine Kinases / drug effects,  genetics,  metabolism*
Rats
Receptor, Epidermal Growth Factor / metabolism
Retroviridae Proteins, Oncogenic / genetics
Signal Transduction
Time Factors
Grant Support
ID/Acronym/Agency:
CA09673-19/CA/NCI NIH HHS; CA44356/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/Culture Media, Serum-Free; 0/Immediate-Early Proteins; 0/Oncogene Protein v-crk; 0/Retroviridae Proteins, Oncogenic; EC 2.7.-/Protein Kinases; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 2.7.10.1/Receptor, Epidermal Growth Factor; EC 2.7.11.17/Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 2.7.12.2/Mitogen-Activated Protein Kinase Kinases; EC 3.1.3.16/Phosphoprotein Phosphatases; EC 3.1.3.16/Protein Phosphatase 1; EC 3.1.3.48/Dual Specificity Phosphatase 1; EC 3.1.3.48/Dusp1 protein, rat; EC 3.1.3.48/Protein Tyrosine Phosphatases

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