| Name | mitogen activated protein kinase (protein family or complex) |
|---|---|
| Synonyms | MAPK; mitogen activated protein kinase; mitogen activated protein kinases |
| Name | sodium azide |
|---|---|
| CAS | sodium azide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 16571865 | Li Z, Hyseni X, Carter JD, Soukup JM, Dailey LA, Huang YC: Pollutant particles enhanced H2O2 production from NAD (P) H oxidase and mitochondria in human pulmonary artery endothelial cells. Am J Physiol Cell Physiol. 2006 Aug;291(2):C357-65. Epub 2006 Mar 29. We hypothesized that PM enhanced oxidative stress in vascular endothelial cells and investigated the enzymatic sources of reactive species and their effects on mitogen-activated protein kinase (MAPK) activation and vasoconstriction. Within minutes after UP treatment, HPAEC increased H2O2 production that could be inhibited by diphenyleneiodonium (DPI), apocynin (APO), and sodium azide (NaN3). |
1(0,0,0,1) | Details |
| 16294328 | Valacco MP, Varone C, Malicet C, Canepa E, Iovanna JL, Moreno S: Cell growth-dependent subcellular localization of p8. J Cell Biochem. 2006 Apr 1;97(5):1066-79. The putative NLS has been demonstrated to be functional, since nuclear import is energy dependent (inhibited by sodium azide plus 2-deoxyglucose), and fusion proteins GFP-p8 and GFP-NLSp8 localize to the nucleus, whereas GFP-p8NLSmut in which with 65, 69, 76, and 77 mutated to localized to the whole cell. p8 localization does not involve the CRM1 transporter, since it is insensitive to leptomycin B. |
0(0,0,0,0) | Details |
| 12945585 | Le Panse R, Dubertret L, Coulomb B: p38 mitogen-activated protein kinase activation by ultraviolet A radiation in human dermal fibroblasts. Photochem Photobiol. 2003 Aug;78(2):168-74. and sodium azide had an inhibitory effect on UVA activation of p38 MAPK, pointing to a role of singlet in transduction of the UVA effect. |
84(1,1,1,4) | Details |
| 9360968 | Yu R, Tan TH, Kong AN: Butylated hydroxyanisole and its metabolite tert-butylhydroquinone differentially regulate mitogen-activated protein kinases. J Biol Chem. 1997 Nov 14;272(46):28962-70. Furthermore, BHA and tBHQ activation of ERK2 was strongly inhibited by and a peroxidase inhibitor, sodium azide, suggesting the potential role of phenoxyl radicals and/or their derivatives. |
4(0,0,0,4) | Details |
| 17384288 | Siniscalchi A, Cavallini S, Marino S, Falzarano S, Franceschetti L, Selvatici R: Effects of chemical ischemia on cerebral cortex slices: focus on mitogen-activated protein kinase cascade. Ann N Y Acad Sci. 2006 Dec;1090:445-54. In superfused, electrically stimulated rat cerebral cortex slices, chemical ischemia (CI) was induced by a 5-min treatment with the mitochondrial toxin, sodium azide (10 mM), combined with the glycolysis blocker, 2-deoxyglucose (2 mM). |
3(0,0,0,3) | Details |
| 19191104 | Kikuchi K, Kohyama T, Yamauchi Y, Kato J, Takami K, Okazaki H, Desaki M, Nagase T, Rennard SI, Takizawa H: C-reactive protein modulates human lung fibroblast migration. Exp Lung Res. 2009 Feb;35(1):48-58. Western blot analysis showed that CRP inhibited the p38 mitogen-activated protein kinase (MAPK) activity in the presence of HFn. |
3(0,0,0,3) | Details |
| 16621957 | Ossum CG, Wulff T, Hoffmann EK: Regulation of the mitogen-activated protein kinase p44 ERK activity during anoxia/recovery in rainbow trout hypodermal fibroblasts. J Exp Biol. 2006 May;209(Pt 9):1765-76. Here we characterise a p44ERK-like protein in the rainbow trout cell line RTHDF and study the effect of (i) serum stimulation, (ii) sodium azide (chemical anoxia) and removal of azide (recovery) and (iii) anoxia (P (O) 2 <0.1%) and recovery. |
2(0,0,0,2) | Details |
| 20032508 | Endale M, Kim SD, Lee WM, Kim S, Suk K, Cho JY, Park HJ, Wagley Y, Kim S, Oh JW, Rhee MH: Ischemia induces regulator of G protein signaling 2 (RGS2) protein upregulation and enhances apoptosis in astrocytes. Am J Physiol Cell Physiol. 2010 Mar;298(3):C611-23. Epub 2009 Dec 23. Upregulated RGS2 was significantly inhibited by SB-203580, a p38 MAPK inhibitor. A marked increase in RGS2 occurred after ischemic stress induced by chemicals (sodium azide and 2-deoxyglucose) or - deprivation (OGD, real ischemia). |
2(0,0,0,2) | 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. Mitochondrial inhibitors such as rotenone, TTFA, antimycin A, sodium azide, oligomycin, and valinomycin were used in this study. Activities of Akt and p38 MAPK, however, were decreased by the inhibitors under deprivation condition except TTFA. |
1(0,0,0,1) | Details |
| 12736272 | Fujimoto TT, Katsutani S, Shimomura T, Fujimura K: Thrombospondin-bound integrin-associated protein (CD47) physically and functionally modifies integrin alphaIIbbeta3 by its extracellular domain. J Biol Chem. 2003 Jul 18;278(29):26655-65. Epub 2003 May 7. Platelet aggregation induced by 4N1K was not completely inhibited by energy depletion with sodium azide and 2-deoxy- although ADP or collagen-induced platelet response was completely inhibited. The truncated form of IAP with only the extracellular immunoglobulin-like (Ig) domain was sufficient for the activation of alphaIIbbeta3 in Chinese hamster ovary cells, although the IAP-mediated intracellular signaling was abolished, which was monitored by the absence of down-regulation of mitogen-activated protein kinase phosphorylation. |
1(0,0,0,1) | Details |