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Портал Begell Электронная Бибилиотека e-Книги Журналы Справочники и Сборники статей Коллекции
Critical Reviews™ in Eukaryotic Gene Expression
Импакт фактор: 1.841 5-летний Импакт фактор: 1.927 SJR: 0.649 SNIP: 0.516 CiteScore™: 1.96

ISSN Печать: 1045-4403
ISSN Онлайн: 2162-6502

Выпуски:
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Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukarGeneExpr.v21.i3.50
pages 291-301

Nuclear Phospholipase C in Biological Control and Cancer

Giulia Ramazzotti
Cellular Signalling Laboratory, Department of Human Anatomical Sciences, University of Bologna, Bologna, Italy
Irene Faenza
Cellular Signalling Laboratory, Department of Human Anatomical Sciences, University of Bologna, Bologna, Italy
Matilde Y. Follo
Cellular Signalling Laboratory, Department of Human Anatomical Sciences, University of Bologna, Bologna, Italy
Roberta Fiume
Cellular Signalling Laboratory, Department of Human Anatomical Sciences, University of Bologna, Bologna, Italy
Manuela Piazzi
Cellular Signalling Laboratory, Department of Human Anatomical Sciences, University of Bologna, Bologna, Italy
Roberto Giardino
Laboratory of Preclinical and Surgical Studies, Rizzoli Orthopedic Institute, Bologna, Italy
Milena Fini
Laboratory of Preclinical and Surgical Studies, Rizzoli Orthopedic Institute, Bologna, Italy
Lucio Cocco
University of Bologna

Краткое описание

Inositol lipids are key regulators of several cellular functions. The identification of an independent nuclear polyphosphoinositides signaling machinery has led the way to find new roles for these molecules. PI-PLC-β1 is the most extensively studied PLC isoform in the nuclear compartment and a key player in the regulation of nuclear lipid signaling. Nuclear PI-PLC-β1 is involved in cell cycle progression and differentiation in response to growth factor stimulation. A growing body of evidence has demonstrated that nuclear phosphoinositides are also involved in cancer cell generation, proliferation, and resistance to apoptosis. Evidence on ex vivo human cancer cells from patients with myelodysplastic syndromes (MDS) confirmed these observations, suggesting the involvement of PI-PLC-β1 both in the pathogenesis of the disease and in the progression of MDS to acute myeloid leukemia. These studies have offered new targets for the development of novel therapeutic strategies as well as new prognostic tools.