| Name | tumor necrosis factor |
|---|---|
| Synonyms | Cachectin; DIF; TNF; TNF alpha; TNF a; TNFA; TNFSF 2; TNFSF2… |
| Name | sodium azide |
|---|---|
| CAS | sodium azide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 11200060 | Heale JP, Speert DP: Protein kinase C agonists enhance phagocytosis of P. aeruginosa by murine alveolar macrophages. J Leukoc Biol. 2001 Jan;69(1):158-60. Furthermore, the addition of PKC agonists, such as phorbol (PMA), and tumor necrosis factor alpha (TNF-alpha), mimicked the phagocytic enhancing effect of sodium azide. |
31(0,1,1,1) | Details |
| 10764744 | Bai J, Cederbaum AI: Overexpression of catalase in the mitochondrial or cytosolic compartment increases sensitivity of HepG2 cells to tumor necrosis factor-alpha-induced apoptosis. J Biol Chem. 2000 Jun 23;275(25):19241-9. Sodium azide, an inhibitor of catalase, reduced the increased sensitivity of mC5 and C33 cells to TNF-alpha to the level of toxicity found with control Hp cells. |
2(0,0,0,2) | Details |
| 7648436 | Fady C, Gardner A, Jacoby F, Briskin K, Tu Y, Schmid I, Lichtenstein A: Atypical apoptotic cell death induced in L929 targets by exposure to tumor necrosis factor. J Interferon Cytokine Res. 1995 Jan;15(1):71-80. In contrast, chromatin condensation and ladder-like DNA fragmentation were not detected in L929 targets dying by necrosis from exposure to heat, repeated cycles of freeze-thaw, and sodium azide. |
2(0,0,0,2) | Details |
| 17531242 | Nabata A, Kuroki M, Ueba H, Hashimoto S, Umemoto T, Wada H, Yasu T, Saito M, Momomura S, Kawakami M: C-reactive protein induces endothelial cell apoptosis and matrix metalloproteinase-9 production in human mononuclear cells: Implications for the destabilization of atherosclerotic plaque. Atherosclerosis. 2008 Jan;196(1):129-35. Epub 2007 May 24. However, recent in vitro studies raised the possibility that the effects of CRP are caused by biologically active contaminants such as sodium azide and endotoxin. In human mononuclear cells, CRP-induced production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and matrix metalloproteinase-9 (MMP-9) in a concentration-dependent manner. |
1(0,0,0,1) | Details |
| 16786153 | Pompili E, Fabrizi C, Fumagalli L: PAR-1 upregulation by trimethyltin and lipopolysaccharide in cultured rat astrocytes. Int J Mol Med. 2006 Jul;18(1):33-9. Furthermore, an evident upregulation of PAR-1 in cultured primary astrocytes also occurred following exposure to lipopolysaccharide (LPS) (a well-known inductor of glial cell activation) whereas other agents (such as staurosporine, peroxide and sodium azide), which are known to induce cell death, were unable to determine any PAR-1 variation. Furthermore, after exposure to TMT and LPS, the levels of tumor necrosis factor-alpha and interleukin-1beta were also increased in astrocyte cultures, suggesting that the PAR-1 upregulation we have detected may be involved in glial inflammatory response rather than in cell death. |
1(0,0,0,1) | Details |
| 11337370 | Doublier S, Ruotsalainen V, Salvidio G, Lupia E, Biancone L, Conaldi PG, Reponen P, Tryggvason K, Camussi G: Nephrin redistribution on podocytes is a potential mechanism for proteinuria in patients with primary acquired nephrotic syndrome. Am J Pathol. 2001 May;158(5):1723-31. This phenomenon was abrogated by cytochalasin and sodium azide. |
0(0,0,0,0) | 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. The Fas/Apo-1 molecule is a member of tumor necrosis factor/nerve growth factor (TNF/NGF) receptor family and is able to induce apoptosis in various type of malignant cells, including most of the human leukemia T-cells. This observation seemed specific to Fas-mediated apoptosis, because ionophore A23187 or sodium azide failed to repress the expression of cdks. |
1(0,0,0,1) | Details |