Among cellular second messengers inositides play key roles in signal transduction pathways. Indeed, nuclear phosphoinositide-specific phospholipase C (PI-PLC) beta 1 and Akt are involved in cell cycle progression and apoptosis. Nuclear lipid metabolism has raised interest in the last years, mainly because of its link with haematopoietic progenitor cells. Myelodysplastic syndromes (MDS) are stem-cell clonal diseases characterized by an impaired hempoiesis and a differentiation defect in one or more of the bone marrow lineages, often leading to progression to acute myeloid leukaemia (AML). The MDS evolution to AML is not completely understood but, at a molecular level, the nuclear inositide signalling pathways can play an important role in this process.
Matilde Y. Follo, Sara Mongiorgi, Carlo Finelli, Manuela Piazzi, Irene Faenza, Giulia Ramazzotti, et al. (2012). Nuclear PI-PLCβ1 and Myelodysplastic Syndromes: Genetics and Epigenetics. CURRENT PHARMACEUTICAL DESIGN, 18(13), 1751-1754 [10.2174/138161212799859710].
Nuclear PI-PLCβ1 and Myelodysplastic Syndromes: Genetics and Epigenetics
FOLLO, MATILDE YUNG;MONGIORGI, SARA;FINELLI, CARLO;PIAZZI, MANUELA;FAENZA, IRENE;RAMAZZOTTI, GIULIA;SANTI, PATRIZIA;MARTELLI, ALBERTO MARIA;COCCO, LUCIO ILDEBRANDO
2012
Abstract
Among cellular second messengers inositides play key roles in signal transduction pathways. Indeed, nuclear phosphoinositide-specific phospholipase C (PI-PLC) beta 1 and Akt are involved in cell cycle progression and apoptosis. Nuclear lipid metabolism has raised interest in the last years, mainly because of its link with haematopoietic progenitor cells. Myelodysplastic syndromes (MDS) are stem-cell clonal diseases characterized by an impaired hempoiesis and a differentiation defect in one or more of the bone marrow lineages, often leading to progression to acute myeloid leukaemia (AML). The MDS evolution to AML is not completely understood but, at a molecular level, the nuclear inositide signalling pathways can play an important role in this process.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.