Abstract:
:The nucleus has been shown to be a site for the inositol lipid cycle that can be affected by treatment of quiescent cells with growth factors such as insulin-like growth factor I (IGF-I). Indeed, the exposure of Swiss 3T3 cells to IGF-I results in a rapid and transient increase in nuclear phospholipase C (PLC) beta1 activity. In addition, several other reports have shown the involvement of PLC beta1 in nuclear signaling in different cell types. Although the demonstration of phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate hydrolysis by nuclear PLC beta1 established the existence of nuclear PLC signaling, the significance of this autonomous pathway in the nucleus has yet to be thoroughly clarified. By inducing both the inhibition of PLC beta1 expression by antisense RNA and its overexpression, we show that this nuclear PLC is essential for the onset of DNA synthesis following IGF-I stimulation of quiescent Swiss 3T3 cells.
journal_name
Cancer Resjournal_title
Cancer researchauthors
Manzoli L,Billi AM,Rubbini S,Bavelloni A,Faenza I,Gilmour RS,Rhee SG,Cocco Lsubject
Has Abstractpub_date
1997-06-01 00:00:00pages
2137-9issue
11eissn
0008-5472issn
1538-7445journal_volume
57pub_type
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