Phospholipase A2 and signal transduction.
نویسندگان
چکیده
منابع مشابه
Receptor-mediated activation of phospholipase A2 and arachidonic acid release in signal transduction.
Neurotransmitters, hormones, cytokines, growth factors and other ligands transmit their specific messages by binding to receptor molecules on the cell surface. The ligand-bound receptors activate effector systems such as adenylate cyclase, cyclic nueleotide phosphodiesterase, ion channels, and phospholipases via membrane-associated transducing systems to generate second messengers. Receptors ac...
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A patient with a mild bleeding disorder whose platelets responded defectively to thromboxane A2 (TXA2) was identified, and the mechanism of this dysfunction was analyzed. The platelets were defective in shape change, aggregation, and release reaction in response to synthetic TXA2 mimetic (STA2). When the platelet TXA2 receptor was examined with both a 125I-labeled derivative of a TXA2 receptor ...
متن کاملDefective Signal Transduction Induced by Thromboxane A2 in a Patient With a Mild Bleeding Disorder: Impaired Phospholipase
A patient with a mild bleeding disorder whose platelets responded defectively to thromboxane A, (TXA,) was identified, and the mechanism of this dysfunction was analyzed. The platelets were defective in shape change, aggregation, and release reaction in response to synthetic TXA, mimetic (STA,). When the platelet TXA, receptor was examined with both a 1251-labeled derivative of a TXA, receptor ...
متن کاملLysosomal phospholipase A2 and phospholipidosis.
A lysosomal phospholipase A2, LPLA2, was recently characterized and shown to have substrate specificity for phosphatidylcholine and phosphatidylethanolamine. LPLA2 is ubiquitously expressed but is most highly expressed in alveolar macrophages. Double conditional gene targeting was employed to elucidate the function of LPLA2. LPLA2-deficient mice (Lpla2-/-) were generated by the systemic deletio...
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ژورنال
عنوان ژورنال: Journal of the American Society of Nephrology
سال: 1992
ISSN: 1046-6673,1533-3450
DOI: 10.1681/asn.v32128