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XB-ART-35215
Science. February 9, 2007; 315 (5813): 840-3.

Integration of TGF-beta and Ras/MAPK signaling through p53 phosphorylation.

Cordenonsi M , Montagner M , Adorno M , Zacchigna L , Martello G , Mamidi A , Soligo S , Dupont S , Piccolo S .


Abstract
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.

PubMed ID: 17234915
Article link: Science.

Genes referenced: mapk1 tgfb1 tp53
Antibodies referenced:
Morpholinos referenced:

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