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phosphatidic acid/sarkom
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Metabolism of phosphatidyl-dCMP in sarcoma 180 cells. Effect of chlorpromazine, phosphatidic acid and inositol.
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The synthesis and degradation of phosphatidyl-dCMP was studied in intact and permeabilized Sarcoma 180 cells as well as in isolated nuclei. It was verified that chlorpromazine greatly enhanced phosphatidyl-dCMP synthesis and completely abolished its hydrolysis in intact cells. The former effect was
Evidence that the Rous sarcoma virus transforming gene product phosphorylates phosphatidylinositol and diacylglycerol.
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The ability of purified Rous sarcoma virus transforming gene product, pp60v-src, to phosphorylate phosphatidylinositol and diacylglycerol was investigated. Phosphatidylinositol was phosphorylated to form both mono- and diphosphorylated derivatives. 1,2-Diacylglycerol was phosphorylated to form
Phospholipids stimulate phosphorylation of vinculin by the tyrosine-specific protein kinase of Rous sarcoma virus.
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The phosphorylation of vinculin by a highly purified tyrosine-specific protein kinase was enhanced more than 10-fold by anionic phospholipids: the phosphorylation of casein, actin, and alpha-actinin was inhibited. The effect of phospholipid was dependent on the divalent cation used. Stimulation was
Inhibition of platelet-derived growth factor-induced cell growth signaling by a short interfering RNA for EWS-Fli1 via down-regulation of phospholipase D2 in Ewing sarcoma cells.
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EWS-Fli1, a fusion gene resulting from a chromosomal translocation t(11;22, q24;q12) and found in Ewing sarcoma and primitive neuroectodermal tumors, encodes a transcriptional activator and promotes cellular transformation. However, the precise biological functions of its products remain unknown. To
Release profiles of recombinant human tumor necrosis factor from Ca(2+)-triggering liposome in vivo.
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After the administration of the recombinant human tumor necrosis factor (rHuTNF), plasma concentration could be controlled from egg yolk phosphatidylcholine (eggPC)-egg yolk phosphatidic acid (eggPA) liposome (EggPA liposome). The plasma concentration was highest after the rHuTNF solution
Formulation, stability, and antitumor activity of 1-beta-D-arabinofuranosylcytosine conjugate of thioether phospholipid.
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1-beta-D-Arabinofuranosylcytosine 5'-diphosphate-rac-1-S-octadecyl-2-O- palmitoyl-1-thioglycerol (ara-CDP-DL-PTBA) is an effective stable 1-beta-D-arabinofuranosylcytosine (ara-C) conjugate of thioether phospholipid against a variety of transplantable tumors in mice. The conjugate was formulated in
Inactivation of (Na-++K-+)-stimulated ATPase by a cytotoxic protein from cobra venom in relation to its lytic effects on cells.
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The mechanism of action of the cytotoxic protein P6 isolated from cobra venom (Naja naja) which shows preferential cytotoxicity particularly to Yoshida sarcoma cells has been studied by its effects on the membrane-bound enzyme (Na-++K-+)-ATPase (ATP phosphohydrolase, EC 3.6.1.3) of a variety of cell
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