Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.2 (guanylate cyclase)
 8,497 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have previously demonstrated that the induction of haem oxygenase-1 (EC 1.14.99.3) plays a protective role for soybean plants against cadmium and UV-B stress. Here, we have investigated the possible signal transduction pathways involved in haem oxygenase-1 induction in leaves of soybean plants subjected to salt stress. Treatment with 100 mM NaCl during 48 h increased thiobarbituric acid reactive substances by 30%, whereas GSH decreased by 50%, with respect to controls. These effects were prevented by pre-incubation with diphenyleneiodonium (DPI; an NADPH oxidase inhibitor), [1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ; a guanylate cyclase inhibitor) or LaCl3 (calcium channel blocker). NaCl at 100 mM produced in situ accumulation of H2O2 and O2*-, which were also prevented by DPI, ODQ or LaCl3. Moreover, salt-induced haem oxygenase-1 activity was also totally abolished by pretreatment with the different inhibitors. These results clearly demonstrated that the signal transduction pathways involved in oxidative stress triggered by salt stress were similar to those implicated in haem oxygenase-1 induction, and provide additional information suggesting that haem oxygenase might play a key role in the antioxidative protection machinery of higher plants.
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PMID:Signal transduction pathways and haem oxygenase induction in soybean leaves subjected to salt stress. 1901 65

Adipose tissue-derived mesenchymal stem cells (ASCs) are a promising stem cell source for cell transplantation. We demonstrate that undifferentiated ASCs display robust oscillations of intracellular calcium [Ca(2+) ](i) which may be associated with stem cell maintenance since oscillations were absent in endothelial cell differentiation medium supplemented with FGF-2. [Ca(2+) ](i) oscillations were dependent on extracellular Ca(2+) and Ca(2+) release from intracellular stores since they were abolished in Ca(2+) -free medium and in the presence of the store-depleting agent thapsigargin. They were inhibited by the phospholipase C antagonist U73,122, the inositol 1,4,5-trisphosphate (InsP(3) ) receptor antagonist 2-aminoethoxydiphenyl borate (2-APB) as well as by the gap-junction uncouplers 1-heptanol and carbenoxolone, indicating regulation by the InsP(3) pathway and dependence on gap-junctional coupling. Cells endogenously generated nitric oxide (NO), expressed NO synthase 1 (NOS 1) and connexin 43 (Cx 43). The nitric oxide NOS inhibitors NG-monomethyl-L-arginine (L-NMMA), N(G)-nitro-L-arginine methyl ester (L-NAME), 2-ethyl-2-thiopseudourea, and diphenylene iodonium as well as si-RNA-mediated down-regulation of NOS 1 synchronized [Ca(2+) ](i) oscillations between individual cells, whereas the NO-donors S-nitroso-N-acetylpenicillamine (SNAP) and sodium nitroprusside (SNP) as well as the soluble guanylate cyclase inhibitor 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ) were without effects. The synchronization of [Ca(2+) ](i) oscillations was due to an improvement of intracellular coupling since fluorescence recovery after photobleaching (FRAP) revealed increased reflow of fluorescent calcein into the bleached area in the presence of the NOS inhibitors DPI and L-NAME. In summary our data demonstrate that intracellular NO levels regulate synchronization of [Ca(2+) ](i) oscillations in undifferentiated ASCs by controlling gap-junctional coupling.
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PMID:NOS inhibition synchronizes calcium oscillations in human adipose tissue-derived mesenchymal stem cells by increasing gap-junctional coupling. 2141 22