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Implications of prostaglandin D2 and leukotrienes in exhaled breath condensates of asthma.

08:00 EDT 12th April 2019 | BioPortfolio

Summary of "Implications of prostaglandin D2 and leukotrienes in exhaled breath condensates of asthma."

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This article was published in the following journal.

Name: Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
ISSN: 1534-4436
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Medical and Biotech [MESH] Definitions

Any tests done on exhaled air.

Cell surface receptors that bind prostaglandins with high affinity and trigger intracellular changes which influence the behavior of cells. Prostaglandin receptor subtypes have been tentatively named according to their relative affinities for the endogenous prostaglandins. They include those which prefer prostaglandin D2 (DP receptors), prostaglandin E2 (EP1, EP2, and EP3 receptors), prostaglandin F2-alpha (FP receptors), and prostacyclin (IP receptors).

Oxidoreductases that catalyze the GLUTATHIONE-dependent oxidoreduction of PROSTAGLANDIN H2 to PROSTAGLANDIN E2.

Cell surface receptors which bind prostaglandins with a high affinity and trigger intracellular changes which influence the behavior of cells. Prostaglandin E receptors prefer prostaglandin E2 to other endogenous prostaglandins. They are subdivided into EP1, EP2, and EP3 types based on their effects and their pharmacology.

Cell-surface receptors that bind LEUKOTRIENES with high affinity and trigger intracellular changes influencing the behavior of cells. The leukotriene receptor subtypes have been tentatively named according to their affinities for the endogenous leukotrienes LTB4; LTC4; LTD4; and LTE4.

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