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Raf‐1 is not a major upstream regulator of MAP kinases in rat fibroblasts
Author(s) -
Kizaka-Kondoh Shinae,
Okayama Hiroto
Publication year - 1993
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(93)80814-b
Subject(s) - kinase , activator (genetics) , mapk/erk pathway , regulator , mitogen activated protein kinase , oncogene , microbiology and biotechnology , biology , p38 mitogen activated protein kinases , cancer research , gene , genetics , cell cycle
RCR cells are NRK clones in which Raf‐1 production is blocked by the expression of an antisense RNA, and consequently they are refractory to transformation by various oncogenes. In RCR cells, MAP kinases (ERK1 and ERK2) were activated to an extent and in a time course similar to those of the original NRK cells, irrespective of whether the stimulus was oncogenic or non‐oncogenic. Moreover, there was no significant elevation of ERK activities in oncogene‐transfonned NRK cells. These results indicate that Raf‐1 kinase is not the major upstream activator of ERK's in NRK cells and that neither ERK1 nor ERK2 are likely to mediate oncogenic signals from Raf‐1 kinase.