Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.4.1 (phosphodiesterase)
 18,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activation of a DNA polymerase delta (pol delta) purified from bovine placenta by ginsenosides from Panax Ginseng C. A. Meyer has been studied. Preincubation of the enzyme with ginsenosides increased the polymerase activity 2.2-fold in a dose-dependent manner. There was a reproducible decrease in Km, in addition to a substantial increase in Vmax, in response to increasing concentrations of ginsenosides. Ginsenosides also activated the proofreading ability of 3'- to 5'-exonuclease activity associated with DNA pol delta. The coordinated activation of both polymerase and exonuclease activities of DNA pol delta by ginsenosides is consistent with the view that its polymerase and its exonuclease activities residue on the same protein molecule. UV/Vis difference spectroscopic studies suggested that the activation of DNA pol delta by ginsenosides might be due to the conformational change induced by ginsenosides binding.
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PMID:Ginsenosides activate DNA polymerase delta from bovine placenta. 756 83

Elevated concentrations of plasma free fatty acids (FFA) may cause insulin resistance. Inhibition of lipolysis reduces FFA availability and improves insulin sensitivity. Ginseng extract (Panax spp., GE) was shown to improve glycemia in Type 2 diabetes. In the present study, the antilipolytic effect of GE in rat adipocytes and the signaling pathway for GE antilipolysis were investigated. Adipocytes were isolated from rat fat tissue by collagenase digestion. The ability of GE to inhibit lipolysis was assessed by measuring glycerol and FFA release into the incubation medium. Phosphatidylinositol 3-kinase (PI3-K) inhibitor and various phosphodiesterase (PDE) inhibitors were applied to investigate the signaling pathway for GE antilipolysis. The present study showed that insulin and GE inhibited lipolysis by 42.4 and 49% compared with basal, respectively (P < 0.05). Unlike insulin, the PI3-K inhibitor wortmannin did not reverse GE antilipolysis, and GE did not affect phosphorylation of protein kinase B (PKB). The nonselective PDE inhibitor enprofylline reversed both insulin and GE antilipolysis. The specific phosphodiesterase 3 (PDE3) inhibitor cilostamide reversed insulin antilipolysis completely, but did not significantly affect GE antilipolysis. The specific phosphodiesterase 4 (PDE4) inhibitor rolipram did not significantly affect insulin antilipolysis, but almost completely reversed GE antilipolysis. Moreover, the combination of PDE3 and PDE4 inhibitors completely reversed GE antilipolysis. None of the ginsenosides (Rb1, Re, Rg1, Rc, Rb2, and Rd) were responsible for GE antilipolysis. The results suggest that ginseng exerts its antilipolytic effect through a signaling pathway different from that of insulin. GE antilipolysis is mediated in part by activating PDE4 in rat adipocytes.
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PMID:Ginseng extract inhibits lipolysis in rat adipocytes in vitro by activating phosphodiesterase 4. 1642 9