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Selective inhibition of receptor-coupled phospholipase C-dependent processes in human platelets and polymorphonuclear neutrophils.
Data are consistent with the observed inhibition by U-73122 of platelet activation by the thromboxane receptor agonist, U-46619, via a mechanism that involves inhibition of a phospholipase C-dependent component(s) of signal transduction. Expand
Inhibition of phospholipase C dependent processes by U-73, 122.
Albumin-catalyzed metabolism of prostaglandin D2. Identification of products formed in vitro.
Results suggest that albumin can influence, qualitatively and quantitatively, the metabolism of eicosanoids. Expand
Regulated formation of eicosanoids.
Several mechanisms through which cells attain more subtle control of eicosanoid biosynthesis are commented on, including saturating amounts of exogenous arachidonic acid ought to reveal all biosynthetic products and pathways. Expand
Pharmacophore model for novel inhibitors of ubiquitin isopeptidases that induce p53-independent cell death.
Using the National Cancer Institute's Developmental Therapeutics Database to identify compounds to test the pharmacophore and mechanism of action hypothesis, data verify the p53-independence of cell death caused by inhibitors of the proteasome pathway and support the proposition that the ubiquitin-dependent proteasom pathway may contain molecular targets suitable for antineoplastic drug discovery. Expand
Inhibition of cyclooxygenase activity and platelet aggregation by epoxyeicosatrienoic acids. Influence of stereochemistry.
The results suggest that effects of EET may originate from either stereospecific or nonspecific mechanisms, and definition of such mechanisms may be important to appreciate any physiological relevance of these substances. Expand
Erythrocyte-neutrophil interactions: formation of leukotriene B4 by transcellular biosynthesis.
Transcellular biosynthesis ofLeukotriene B4 from erythrocyte-neutrophil interactions explains the paradoxical presence of leukotRIene A4 hydrolase within ery Throcytes, a cell incapable of synthesizing leukosanoid biosynthesis; indicates that the biosynthetic capacity of cell combinations is not necessarily equivalent to the sum of their separate capacities. Expand
Cyclooxygenase-2 and carcinogenesis.
This set of findings seems to link very strongly with the traditional observation that chronic inflammation is a precursor to a variety of types of cancer, by this formulation, inflammatory stimuli increase COX-2 and the downstream events that it induces promote tumor formation. Expand
Cyclooxygenase enzymes: regulation and function.
  • F. Fitzpatrick
  • Chemistry, Medicine
  • Current pharmaceutical design
  • 31 January 2004
This review discusses how two separate catalytic processes in COX act in an integrated fashion manner to generate prostaglandin synthase and why irreversible inactivation of COX is important constitutively and pharmacologically and how cells have managed to use two closely related, almost identical enzymes in ways that discriminate their physiological versus pathological roles. Expand
Inhibition of 5-lipoxygenase-activating protein (FLAP) reduces pulmonary vascular reactivity and pulmonary hypertension in hypoxic rats.
The hypothesis that the 5-LO is involved in lung vascular tone regulation and in the development of chronic pulmonary hypertension in hypoxic rodent models is supported. Expand