Mitogen-Activated Protein Kinase Activation Resulting from Selective Oncogene Expression in NIH 3T3 and Rat 1a Cells

Mitogen-Activated Protein Kinase Activation Resulting from Selective Oncogene Expression in NIH 3T3 and Rat 1a Cells

Mitogen-activated protein kinases (MAPKs) are serine/threonine kinases that are rapidly activated in response to a variety of growth factors in many cell types. MAPKs are activated by phosphorylation of both tyrosine and threonine residues. They are proposed to be key integrators of growth factor re...

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Veröffentlicht in:Proceedings of the National Academy of Sciences of the United States of America. - National Academy of Sciences of the United States of America. - 89(1992), 16, Seite 7355-7359
1. Verfasser: Gallego, Carme (VerfasserIn)
Weitere Verfasser: Gupta, Sunil K., Heasley, Lynn E., Qian, Nan-Xin, Johnson, Gary L.
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 1992
Zugriff auf das übergeordnete Werk:Proceedings of the National Academy of Sciences of the United States of America
Schlagworte:Cell Biology Transformation Protein Kinases Oncoproteins Biological sciences Physical sciences
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520 |a Mitogen-activated protein kinases (MAPKs) are serine/threonine kinases that are rapidly activated in response to a variety of growth factors in many cell types. MAPKs are activated by phosphorylation of both tyrosine and threonine residues. They are proposed to be key integrators of growth factor receptor transduction systems involving conversion of tyrosine kinase signals to serine/threonine kinase activation. We have studied the influence of specific oncogenes on the regulation of MAPK activity in NIH 3T3 and Rat 1a fibroblasts. In NIH 3T3 cells, ras or raf oncogene expression, but not gip2 oncogene expression, induces a significant constitutive MAPK activation. In contrast, in Rat 1a cells, gip2, but not ras or raf oncogene expression, induces a strong constitutive MAPK activation. The findings indicate that, in a cell type-selective manner, different oncoproteins are capable of causing the constitutive activation of MAPK. However, the magnitude of oncogene-induced MAPK activation is not directly correlated with cellular transformation in either cell type. It appears that expression of only a subset of transforming oncogenes in a specific cell type is able to alter the regulation of the MAPK activation pathway. Thus, the network of cytoplasmic serine/threonine kinases will be differentially regulated when the same oncogene is expressed in different cell types. 
540 |a Copyright 1992 The National Academy of Sciences of the United States of America 
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700 1 |a Heasley, Lynn E.  |e verfasserin  |4 aut 
700 1 |a Qian, Nan-Xin  |e verfasserin  |4 aut 
700 1 |a Johnson, Gary L.  |e verfasserin  |4 aut 
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