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SB-505124 is a selective inhibitor of transforming growth factor-beta type I receptors ALK4, ALK5, and ALK7.
TLDR
This compound selectively and concentration-dependently inhibits ALK4-, ALK5-, and ALK 7-dependent activation of downstream cytoplasmic signal transducers, Smad2 and Smad3, and of TGF-beta-induced mitogen-activated protein kinase pathway components but does not alter ALK1, ALK2, AlK3 or ALK6-induced Smad signaling. Expand
Mice lacking Smad3 are protected against cutaneous injury induced by ionizing radiation.
TLDR
Inhibition of Smad3 might decrease tissue damage and reduce fibrosis after exposure to ionizing irradiation, as did mice exposed to whole-body irradiation. Expand
Interference with transforming growth factor-beta/ Smad3 signaling results in accelerated healing of wounds in previously irradiated skin.
TLDR
The data suggest that attenuation of Smad3 signaling might improve the healing of wounds in previously irradiated skin commensurate with an inhibition of fibrosis. Expand
Diacylglycerol hydrolysis to arachidonic acid is necessary for insulin secretion from isolated pancreatic islets: sequential actions of diacylglycerol and monoacylglycerol lipases.
TLDR
It is shown that diacylglycerol, a product of phospholipase C action, is a major source of free arachidonic acid in islets and is markedly inhibits glucose- and carbachol-induced increases in islet arachIDonic acid levels, as measured by gas chromatography with electron-capture detection of its pentafluorobenzyl esters. Expand
Extracellular Mediators in Atherosclerosis and Thrombosis: Lessons From Thrombin Receptor Knockout Mice
TLDR
Experimental evidence gleaned from PAR−/− mouse models as well as how the use of PAR+/− mice has provided insights toward understanding the physiological role of thrombin in cells of the vascular system and vascular pathology are examined. Expand
Carbachol stimulation of phospholipase A2 and insulin secretion in pancreatic islets.
TLDR
It is shown, for the first time, that the muscarinic agonist carbachol, at concentrations which stimulate insulin secretion, causes a rapid and nearly 3-fold increase in arachidonic acid accumulation in islets. Expand
Inhibition of phospholipase A2 and insulin secretion in pancreatic islets.
TLDR
The observations suggest that glucose-induced arachidonate increase is essential for insulin secretion, which is specific for phospholipase A2. Expand
Transient activation of calcium-dependent phospholipase A2 by insulin secretagogues in isolated pancreatic islets.
TLDR
It is suggested that activation of islet Ca(2+)-dependent phospholipase A2 may be important in a distal process of insulin secretion, such as secretory granule exocytosis. Expand
Interleukin-1beta stimulation of c-Jun NH(2)-terminal kinase activity in insulin-secreting cells: evidence for cytoplasmic restriction.
TLDR
Data indicate that IL-1beta-stimulated JNK activity may be distinctly targeted to cytoplasmic and/or membrane compartments in clonal insulin-producing cells, and that JNK-interacting protein (JIP) may serve to localize J NK activity to specific substrates. Expand
U-73122 does not specifically inhibit phospholipase C in rat pancreatic islets and insulin-secreting beta-cell lines.
TLDR
Observations suggest that U-73122 does not specifically inhibit phospholipase C in insulin-secreting cells. Expand
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