| Name | bcl 2 |
|---|---|
| Synonyms | Apoptosis regulator Bcl 2; B cell CLL/lymphoma 2; B cell lymphoma protein 2 alpha; B cell lymphoma protein 2 alpha isoform; BCL2; Bcl 2; B cell CLL/lymphoma 2s; B cell lymphoma protein 2 alphas… |
| Name | sodium azide |
|---|---|
| CAS | sodium azide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 11596115 | Del Bufalo D, Trisciuoglio D, Biroccio A, Marcocci L, Buglioni S, Candiloro A, Scarsella M, Leonetti C, Zupi G: Bcl-2 overexpression decreases BCNU sensitivity of a human glioblastoma line through enhancement of catalase activity. J Cell Biochem. 2001 Aug 21-Sep 5;83(3):473-83. The ability of the catalase inhibitor, sodium azide, to increase the BCNU sensitivity of the bcl-2 transfectants to levels of the BCNU-treated control clone substantiated the role of the catalase activity. |
38(0,1,1,8) | Details |
| 8743413 | Vaux DL, Whitney D, Weissman IL: Activation of physiological cell death mechanisms by a necrosis-causing agent. Microsc Res Tech. 1996 Jun 15;34(3):259-66. Although all cells treated with sodium azide showed changes typical of necrosis, in the absence of Bcl-2 the cells died more rapidly and also displayed features of apoptosis. |
10(0,0,1,5) | Details |
| 11193033 | Benitez-Bribiesca L, Gomez-Camarillo M, Castellanos-Juarez E, Mravko E, Sanchez-Suarez P: Morphologic, biochemical and molecular mitochondrial changes during reperfusion phase following brief renal ischemia. Ann N Y Acad Sci. 2000;926:165-79. Ischemia/reperfusion of organs and cells induces apoptosis through a complicated series of changes in mitochondria, mainly the generation of free radicals, permeability transitions, translocations, and release of apoptogenic factors such as cytochrome c and Bcl-2 family members. A model of chemical hypoxia with intra-arterial 50 mM sodium azide served as comparison, allowing free blood flow for 30, 60, 120 and 180 min. |
5(0,0,0,5) | Details |
| 15004018 | Wang J, Wei Q, Wang CY, Hill WD, Hess DC, Dong Z: Minocycline up-regulates Bcl-2 and protects against cell death in mitochondria. J Biol Chem. 2004 May 7;279(19):19948-54. Epub 2004 Mar 5. |
5(0,0,0,5) | Details |
| 8593745 | Vaux DL, Hacker G: Hypothesis: apoptosis caused by cytotoxins represents a defensive response that evolved to combat intracellular pathogens. Clin Exp Pharmacol Physiol. 1995 Nov;22(11):861-3. In most cases, the mechanism of cell death is likely to be the same, as expression of the cell death inhibitory gene bcl-2 can frequently prevent apoptotic changes and/or delay cell death. 2. Experiments on the effect of sodium azide upon growth factor-dependent cells support this idea. |
3(0,0,0,3) | Details |
| 18563357 | Han M, Im DS: Effects of mitochondrial inhibitors on cell viability in U937 monocytes under deprivation. Arch Pharm Res. 2008 Jun;31(6):749-57. Epub 2008 Jun 19. And also activation of JNK, inactivation of ERK, and enhanced expression of Bcl-2 were observed. Mitochondrial inhibitors such as rotenone, TTFA, antimycin A, sodium azide, oligomycin, and valinomycin were used in this study. |
1(0,0,0,1) | Details |
| 20036216 | Hur J, Lee P, Kim MJ, Kim Y, Cho YW: Ischemia-activated microglia induces neuronal injury via activation of gp91phox oxidase. Biochem Biophys Res Commun. 2010 Jan 15;391(3):1526-30. Epub 2009 Dec 28. MCM-treated SH-SY5Y cells showed reduced the viability, increased caspase-3 activity, decreased Bcl-2/Bax ratio, and increased cytochrome c release, increased inflammatory cytokines, and increased reactive species (ROS) generation. |
1(0,0,0,1) | Details |
| 7945420 | Liu Y, Bhalla K, Hill C, Priest DG: Evidence for involvement of phosphorylation in taxol-induced apoptosis in a human ovarian tumor cell line. Biochem Pharmacol. 1994 Sep 15;48(6):1265-72. The specific protein tyrosine kinase inhibitors and herbimycin A, and the ATP depletion agent sodium azide, interfered with taxol-induced DNA fragmentation and clonal cell death. Based on a quantitative reverse transcription-polymerase chain reaction technique, bcl-2 alpha oncogene expression was decreased in conjunction with taxol-induced DNA fragmentation, and this decrease could be blocked by |
1(0,0,0,1) | Details |
| 8788121 | Oguri-Hyakumachi N, Takahashi S, Nakagawa T, Kikuchi K: Selective depletion of cyclin-dependent kinases is associated with Fas-mediated apoptosis in human leukemia T-cell lines. Int J Immunopharmacol. 1995 Nov;17(11):913-21. This observation seemed specific to Fas-mediated apoptosis, because ionophore A23187 or sodium azide failed to repress the expression of cdks. |
0(0,0,0,0) | Details |