Loss of response to transforming growth factor-beta (TGF-β) is thought to contribute to the progression of chronic lymphocytic leukemia. FKBP12-knockout mouse show an over-activation of the TGF-β signal; our findings demonstrate that most chronic lymphocytic leukemia cells escape the homeostatic control of TGF-β and that FK506, the canonical ligand of FKBP, can activate the TGF-β signal and restores the signal in a proportion of non-responsive samples. We particularly demonstrate that FK506 activates the TGF-β receptor I kinase activity, which transduces apoptosis by a mitochondrial-dependent pathway.
FKBP12 controls tumor response to TGF-β induced apoptosis / Romano, Simona. - (2007). (Intervento presentato al convegno VII Molecular Meeting Of Molecular Oncology tenutosi a Positano, Italy nel May 9-12 2007).
FKBP12 controls tumor response to TGF-β induced apoptosis
ROMANO SIMONA
2007
Abstract
Loss of response to transforming growth factor-beta (TGF-β) is thought to contribute to the progression of chronic lymphocytic leukemia. FKBP12-knockout mouse show an over-activation of the TGF-β signal; our findings demonstrate that most chronic lymphocytic leukemia cells escape the homeostatic control of TGF-β and that FK506, the canonical ligand of FKBP, can activate the TGF-β signal and restores the signal in a proportion of non-responsive samples. We particularly demonstrate that FK506 activates the TGF-β receptor I kinase activity, which transduces apoptosis by a mitochondrial-dependent pathway.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
