The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

Editor

Share

Personal info

View

Links

About

Terms

 

 
 

Lipid metabolism in fibroblast growth factor-stimulated L6 myoblasts: a receptor mutation (Y766F) abrogates phospholipase D and diacylglycerol kinase activities.

Phosphatidylcholine (PC) hydrolysis induced by basic fibroblast growth factor (bFGF) was studied in rat L6 myoblasts expressing the wild-type FGF receptor-1 (FGFR-1) or a mutant (Y766F) that is incapable of activating phospholipase C-gamma (PLCgamma). Stimulation of FGFR-1 activated phospholipase D ( PLD) rapidly and transiently, but did not induce PC-specific PLC activity. Downregulation of protein kinase C blocked bFGF- induced PLD activation but not phosphatidic acid formation by diacylglycerol (DG) kinase. Only phosphoinositide (PI)-derived DG, not PC-derived DG, appeared to be a substrate for DG kinase. Stimulation of FGFR-1(Y766F) did not activate PLD or DG kinase, both of which apparently require initial PLCgamma activation. The Y766F mutation reduced mitogen-activated protein kinase activation but not cell proliferation. We conclude that both PI turnover and PC hydrolysis are dispensable for bFGF-induced mitogenesis.[1]

References

  1. Lipid metabolism in fibroblast growth factor-stimulated L6 myoblasts: a receptor mutation (Y766F) abrogates phospholipase D and diacylglycerol kinase activities. van Dijk, M.C., van Blitterswijk, W.J. Biochim. Biophys. Acta (1998) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
 
WikiGenes - Universities