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Ragazzon B et al. – PRKAR1A silencing decreased the percentage of apoptotic cells and the cleavage of apoptosis mediators [caspase–3, poly(ADP–ribose) polymerase, and lamin A/C]. Inactivating mutations of PRKAR1A observed in adrenocortical tumors alter SMAD3, leading to resistance to TGFbeta–induced apoptosis. This cross–talk between the PKA and the TGFbeta signaling pathways reveals a new mechanism of endocrine tumorigenesis.

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