When ectopically expressed, the serine/threonine kinase Mos can induce onco
genic transformation of somatic cells by direct phosphorylation of MAP kina
se/ERK kinase (MEK1), activating the mitogen-activated protein kinases ERK1
and ERK2. On the other hand, overexpression of Mos in C2C12 myoblasts is n
ot transforming. Mos activates myogenic differentiation by promoting hetero
dimerization of the MyoD/E12 proteins, increasing the expression of myogeni
c markers and the positive autoregulatory loop of MyoD. In this study, we s
how that in myogenic cells, the mitogenic and oncogenic signalling from the
Mos/MEK/ERK pathway is suppressed by MyoD through the formation of a heter
otrimeric complex. (C) 1999 Federation of European Biochemical Societies.