Abstract：
:Constitutive expression of the activated Rap1A protein inhibits differentiation of myogenic C2 cells whereas the inactivated Rap1A protein favours cell differentiation and induces late endocytic compartments clustering. Although the role of Rap1A in MAPK activation has been analysed in various cell types, the signalling pathways activated by Rap1A have not been explored in myogenic cells. In this study, we investigated MAP kinase activity in control C2 myoblasts and in stable C2 cell lines expressing mutated Rap1A proteins. We provide evidence that Rap1A mutants promote ERK activation and that the active protein induces a more sustained activation than the inactive protein. In addition, we established that various pathways mediate transient ERK activation in control cells and in cells expressing the inactivated Rap1A protein. In these cells, ERK are activated by a Raf/MEK-dependent pathway, a P13K/Raf-independent pathway and a third undetermined pathway. In cells expressing the activated Rap1A protein, a PI3K/Raf/MEK-dependent pathway mediates transient ERK activation. However, MAPK activation appears more complex since, according to the state of the myoblasts or the duration of MAPK stimulation, we observed that Rap1A protein could interfere or not with ERK activation.
journal_name
Oncogenejournal_title
Oncogeneauthors
Pizon V,Baldacci Gdoi
10.1038/sj.onc.1203984subject
Has Abstractpub_date
2000-12-07 00:00:00pages
6074-81issue
52eissn
0950-9232issn
1476-5594journal_volume
19pub_type
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