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Journal Abstract Search
215 related items for PubMed ID: 3117799
1. Phosphatidate accumulation in hormone-treated hepatocytes via a phospholipase D mechanism. Bocckino SB, Blackmore PF, Wilson PB, Exton JH. J Biol Chem; 1987 Nov 05; 262(31):15309-15. PubMed ID: 3117799 [Abstract] [Full Text] [Related]
2. Ca2+-mobilizing hormones elicit phosphatidylethanol accumulation via phospholipase D activation. Bocckino SB, Wilson PB, Exton JH. FEBS Lett; 1987 Dec 10; 225(1-2):201-4. PubMed ID: 3319693 [Abstract] [Full Text] [Related]
3. Hormonal stimulation of diacylglycerol formation in hepatocytes. Evidence for phosphatidylcholine breakdown. Augert G, Bocckino SB, Blackmore PF, Exton JH. J Biol Chem; 1989 Dec 25; 264(36):21689-98. PubMed ID: 2513325 [Abstract] [Full Text] [Related]
7. Stimulation of phosphatidate synthesis in endothelial cells in response to P2-receptor activation. Evidence for phospholipase C and phospholipase D involvement, phosphatidate and diacylglycerol interconversion and the role of protein kinase C. Purkiss JR, Boarder MR. Biochem J; 1992 Oct 01; 287 ( Pt 1)(Pt 1):31-6. PubMed ID: 1417783 [Abstract] [Full Text] [Related]
13. P2-purinergic agonists stimulate phosphodiesteratic cleavage of phosphatidylcholine in endothelial cells. Evidence for activation of phospholipase D. Martin TW, Michaelis K. J Biol Chem; 1989 May 25; 264(15):8847-56. PubMed ID: 2722803 [Abstract] [Full Text] [Related]
14. Effects of pertussis toxin on extracellular signal-regulated kinase activation in hepatocytes by hormones and receptor-independent agents: evidence suggesting a stimulatory role of G(i) proteins at a level distal to receptor coupling. Melien O, Sandnes D, Johansen EJ, Christoffersen T. J Cell Physiol; 2000 Jul 25; 184(1):27-36. PubMed ID: 10825231 [Abstract] [Full Text] [Related]
15. Role of diacylglycerol (DAG) in hormonal induction of S phase in hepatocytes: the DAG-dependent protein kinase C pathway is not activated by epidermal growth factor (EGF), but is involved in mediating the enhancement of responsiveness to EGF by vasopressin, angiotensin II, and norepinephrine. Dajani OF, Sandnes D, Melien O, Rezvani F, Nilssen LS, Thoresen GH, Christoffersen T. J Cell Physiol; 1999 Aug 25; 180(2):203-14. PubMed ID: 10395290 [Abstract] [Full Text] [Related]