Nuclear Phosphatidylinositol Signaling: Focus on Phosphatidylinositol Phosphate Kinases and Phospholipases C.

Citation data:

Journal of cellular physiology, ISSN: 1097-4652, Vol: 231, Issue: 8, Page: 1645-55

Publication Year:
2016
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Repository URL:
http://scholarworks.unist.ac.kr/handle/201301/19288
PMID:
26626942
DOI:
10.1002/jcp.25273
Author(s):
Poli, Alessandro; Billi, Anna Maria; Mongiorgi, Sara; Ratti, Stefano; McCubrey, James A.; Suh, Pann-Ghill; Cocco, Lucio; Ramazzotti, Giulia
Publisher(s):
Wiley; WILEY-BLACKWELL
Tags:
Biochemistry, Genetics and Molecular Biology; RISK MYELODYSPLASTIC SYNDROMES; CELL-CYCLE PROGRESSION; ACUTE MYELOID-LEUKEMIA; GROWTH-FACTOR-I; MURINE ERYTHROLEUKEMIA-CELLS; SWISS 3T3-CELLS; MESSENGER-RNA; MYOGENIC DIFFERENTIATION; ERYTHROID-DIFFERENTIATION; 4-PHOSPHATE 5-KINASE
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review description
Phosphatidylinositol (PI) metabolism represents the core of a network of signaling pathways which modulate many cellular functions including cell proliferation, cell differentiation, apoptosis, and membrane trafficking. An array of kinases, phosphatases, and lipases acts on PI creating an important number of second messengers involved in different cellular processes. Although, commonly, PI signaling was described to take place at the plasma membrane, many evidences indicated the existence of a PI cycle residing in the nuclear compartment of eukaryotic cells. The discovery of this mechanism shed new light on many nuclear functions, such as gene transcription, DNA modifications, and RNA expression. As these two PI cycles take place independently of one another, understanding how nuclear lipid signaling functions and modulates nuclear output is fundamental in the study of many cellular processes. J. Cell. Physiol. 231: 1645-1655, 2016. © 2015 Wiley Periodicals, Inc.