Abstract
Aims: SMAD proteins have been implicated as downstream effectors of TGFβ/BMP signaling. TGFß activates receptors on the cell surface, stimulating the phosphorylation of receptor-regulated SMAD proteins, which then form complexes with SMAD4 that accumulate in the nucleus and activate TGFß responsive gene transcription (e.g. Collagen-I, WAF-1). SMAD4 is inactivated in 50% of the pancreatic adenocarcinomas.
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