Integration of TGF-beta and Ras/MAPK signaling through p53 phosphorylation
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
During development and tissue homeostasis, cells must integrate different signals. We investigated how cell behavior is controlled by the combined activity of transforming growth factor-beta (TGF-beta) and receptor tyrosine kinase (RTK) signaling, whose integration mechanism is unknown. We find that RTK/Ras/MAPK (mitogen-activated protein kinase) activity induces p53 N-terminal phosphorylation, enabling the interaction of p53 with the TGF-beta-activated Smads. This mechanism confines mesoderm specification in Xenopus embryos and promotes TGF-beta cytostasis in human cells. These data indicate a mechanism to allow extracellular cues to specify the TGF-beta gene-expression program.
Originalsprog | Engelsk |
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Tidsskrift | Science (New York, N.Y.) |
Vol/bind | 315 |
Udgave nummer | 5813 |
Sider (fra-til) | 840-3 |
Antal sider | 4 |
ISSN | 0036-8075 |
DOI | |
Status | Udgivet - 9 feb. 2007 |
Eksternt udgivet | Ja |
ID: 46502265