ArticleJapanese journal of cancer research : Gann2002
Overexpression of phosphatidylinositol synthase enhances growth and G1 progression in NIH3T3 cells.
Article in Japanese journal of cancer research : Gann, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 15 citations in OpenAlex.
- Clinical significance of phosphatidyl inositol synthase overexpression in oral cancer.BMC cancer · 2010Article
- Effect of dietary monosodium glutamate on trans fat-induced nonalcoholic fatty liver disease.Journal of lipid research · 2009Article
- Genomic analysis of PIS1 gene expression.Eukaryotic cell · 2005Article
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5 authors at 2 institutions in 2 countries.
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Abstract
Phosphatidylinositol (PI) turnover is thought to play an important role in the regulation of cell growth. PI synthase (PIS, cytidine diphosphate (CDP)-diacylglycerol (DG): myo-inositol 3-phosphatidyltransferase, EC 2.7.8.11) acts at the last step in the de novo biosynthesis of PI by catalyzing the condensation of CDP-DG and myo-inositol. To study the physiological role of PIS, we established murine NIH3T3 fibroblasts that stably overexpress PIS, by transfection with PIS cDNA (NIH-PIS cells). In immunofluorescence assays, the constitutively overexpressed PIS was found to be localized in the endoplasmic reticulum, as previously reported for the native enzyme activity. NIH-PIS cells showed an increase in PI synthesis in vitro and in vivo, as well as increased cellular levels of PI-4,5-P2 and PI-3,4,5-P3. They also displayed a decrease in their doubling time and accelerated G1 progression. Overexpression of PIS increased cellular levels of the cyclin D1 and E proteins and Akt kinase activity in serum-stimulated quiescent NIH3T3 cells. Moreover, PIS overexpression potentiated the colony formation of NIH3T3 cells in soft agar. These results suggest that PIS accelerates G1 progression and stimulates growth by increasing cellular levels of cyclins D1 and E.
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