| Name | caspase 3 |
|---|---|
| Synonyms | Apopain; CASP 3; CASP3; CPP 32; CPP32; CPP32B; Caspase 3; Caspase 3 precursor… |
| Name | sodium cyanide |
|---|---|
| CAS | sodium cyanide (Na(CN)) |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 14730895 | Zhang JJ, Shi RL: [Effects of caspases on cerebromicrovascular endothelial cell apoptosis induced by hypoxia]. Yao Xue Xue Bao. 2003 Oct;38(10):739-42. The expression of caspase-3 was detected by immunocytochemical method. |
4(0,0,0,4) | Details |
| 14674700 | Kiang JG, Warke VG, Tsokos GC: NaCN-induced chemical hypoxia is associated with altered gene expression. Mol Cell Biochem. 2003 Dec;254(1-2):211-6. Sodium cyanide (NaCN)-induced chemical hypoxia is known to increase intracellular free concentration and reduce cell survival, but its effect on gene expression has not been studied. The NaCN-induced hypoxia was also found to increase caspase-3 cellular activity in both cell types. |
3(0,0,0,3) | Details |
| 17157201 | Sanelli T, Strong MJ: Loss of -mediated down-regulation of NMDA receptors in neurofilament aggregate-bearing motor neurons in vitro: implications for motor neuron disease. Free Radic Biol Med. 2007 Jan 1;42(1):143-51. Epub 2006 Oct 20. To examine neurofilament (NF) aggregate-mediated sensitization of motor neurons to excitotoxicity, we examined NMDA receptor expression and the impact of NO donors (NOC12 or NOC5) or sodium cyanide (NaCN) on influx and viability in dissociated motor neurons derived from wt and hNFL+/+ (NF aggregate-forming) mice. Alterations in intracellular were assayed using Oregon Green dye and the extent of apoptosis using active caspase-3 immunoreactivity. |
1(0,0,0,1) | Details |
| 12606726 | Niquet J, Baldwin RA, Allen SG, Fujikawa DG, Wasterlain CG: Hypoxic neuronal necrosis: protein synthesis-independent activation of a cell death program. Proc Natl Acad Sci U S A. 2003 Mar 4;100(5):2825-30. Epub 2003 Feb 26. Early mitochondrial swelling and loss of the mitochondrial membrane potential were accompanied by release of cytochrome c and followed by caspase-9-dependent activation of caspase-3. |
3(0,0,0,3) | Details |
| 12176748 | Li F, Mao HP, Ruchalski KL, Wang YH, Choy W, Schwartz JH, Borkan SC: Heat stress prevents mitochondrial injury in ATP-depleted renal epithelial cells. Am J Physiol Cell Physiol. 2002 Sep;283(3):C917-26. To test these hypotheses, renal epithelial cells were transiently ATP depleted with sodium cyanide and 2-deoxy- in the absence of medium Concomitant with mitochondrial cytochrome c leak, a seven- to eightfold increase in caspase 3 activity was observed. |
2(0,0,0,2) | Details |
| 16697116 | Niquet J, Seo DW, Allen SG, Wasterlain CG: Hypoxia in presence of blockers of excitotoxicity induces a caspase-dependent neuronal necrosis. Neuroscience. 2006 Aug 11;141(1):77-86. Epub 2006 May 11. They showed early mitochondrial swelling, loss of mitochondrial membrane potential and cytoplasmic release of cytochrome c, followed by activation of caspase-9, and by caspase-9-dependent activation of caspase-3. |
1(0,0,0,1) | Details |
| 18079278 | Kiang JG, Krishnan S, Lu X, Li Y: Inhibition of inducible synthase protects human T cells from hypoxia-induced apoptosis. Mol Pharmacol. 2008 Mar;73(3):738-47. Epub 2007 Dec 13. Sodium cyanide-induced chemical hypoxia triggers a series of biochemical alterations leading to apoptosis in many cell types, including T cells. The inhibition of iNOS limited T-cell apoptosis by decreasing the activity of caspase-3 without affecting the expression of Fas/Apo-1/CD95 on the surface membrane of T cells. |
1(0,0,0,1) | Details |
| 16859701 | Hsieh YC, Yu HP, Suzuki T, Choudhry MA, Schwacha MG, Bland KI, Chaudry IH: Upregulation of mitochondrial respiratory complex IV by estrogen receptor-beta is critical for inhibiting mitochondrial apoptotic signaling and restoring cardiac functions following trauma-hemorrhage. J Mol Cell Cardiol. 2006 Sep;41(3):511-21. Epub 2006 Jul 21. Inhibition of MRC-IV in DPN-treated T-H rats by SCN abolished the DPN-mediated cardioprotection, ATP production, mitochondrial cytochrome c release, caspase-3 cleavage, and apoptosis. |
1(0,0,0,1) | Details |
| 10037476 | Boullerne AI, Nedelkoska L, Benjamins JA: Synergism of and iron in killing the transformed murine oligodendrocyte cell line N20.1. J Neurochem. 1999 Mar;72(3):1050-60. Based on two observations, (a) potentiation of the cytotoxic effect of SNP when coincubated with ferricyanide or ferrocyanide, but not sodium cyanide, and (b) protection by deferoxamine, an iron chelator, we conclude that the greater sensitivity of N20.1 cells to SNP compared with SNAP is due to synergism between NO released and the iron portion of SNP, with the accounting for very little of the cytotoxicity. |
0(0,0,0,0) | Details |