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MyoD binds to Mos and inhibits the Mos/MAP kinase pathway
Author(s) -
Solhonne Brigitte,
Lenormand Jean Luc,
Pelpel Karine,
Leibovitch Marie Pierre,
Leibovitch Serge A.
Publication year - 1999
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/s0014-5793(99)01430-1
Subject(s) - myod , c2c12 , microbiology and biotechnology , mapk/erk pathway , kinase , mitogen activated protein kinase kinase , mitogen activated protein kinase , map kinase kinase kinase , chemistry , pitx2 , protein kinase a , biology , myocyte , myogenesis , biochemistry , transcription factor , gene , homeobox
When ectopically expressed, the serine/threonine kinase Mos can induce oncogenic transformation of somatic cells by direct phosphorylation of MAP kinase/ERK kinase (MEK1), activating the mitogen‐activated protein kinases ERK1 and ERK2. On the other hand, overexpression of Mos in C2C12 myoblasts is not transforming. Mos activates myogenic differentiation by promoting heterodimerization of the MyoD/E12 proteins, increasing the expression of myogenic markers and the positive autoregulatory loop of MyoD. In this study, we show that in myogenic cells, the mitogenic and oncogenic signalling from the Mos/MEK/ERK pathway is suppressed by MyoD through the formation of a heterotrimeric complex.