| Name | protein kinase C (protein family or complex) |
|---|---|
| Synonyms | Protein kinase C; PKC |
| Name | sodium azide |
|---|---|
| CAS | sodium azide |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 7582827 | Bennett MC, Fordyce DE, Rose GM, Wehner JM: Chronic sodium azide treatment decreases membrane-bound protein kinase C activity in the rat hippocampus. Neurobiol Learn Mem. 1995 Sep;64(2):187-90. The present experiment tested the hypothesis that chronic sodium azide treatment might also alter protein kinase C activation. |
38(0,1,2,3) | Details |
| 10619578 | Orie NN, Zidek W, Tepel M: Reactive species in essential hypertension and non-insulin-dependent diabetes mellitus. Am J Hypertens. 1999 Dec;12(12 Pt 1-2):1169-74. ROS was monitored with the dye, dihydrorhodamine-123 (DHR; 1 micromol/L) in the presence or absence of superoxide dismutase scavenger), sodium azide (singlet / peroxide scavenger), kinase inhibitor), or bisindolylmaleimide (protein kinase C inhibitor). |
31(0,1,1,1) | Details |
| 16144060 | McBane J, Santerre P, Labow R: Role of protein kinase C in the monocyte-derived macrophage-mediated biodegradation of polycarbonate-based polyurethanes. J Biomed Mater Res A. 2005 Jul 1;74(1):1-12. |
2(0,0,0,2) | Details |
| 10213179 | Pedreno J, Vila M, Masana L: Mechanisms for regulating platelet high density lipoprotein type3 binding sites: evidence that binding sites are downregulated by a protein kinase C-dependent mechanism. Thromb Res. 1999 Apr 1;94(1):33-44. Nevertheless, neither inhibitors of binding sites recycling or of pinocytosis, such as ammonium chloroquine, monensin, colchicine, and sodium azide, modified the binding characteristics. |
2(0,0,0,2) | Details |
| 15064160 | Okai Y, Sato EF, Higashi-Okai K, Inoue M: Enhancing effect of the endocrine disruptor para-nonylphenol on the generation of reactive species in human blood neutrophils. Environ Health Perspect. 2004 Apr;112(5):553-6. -dependent oxidase inhibitor, diphenyl iodonium and the myeloperoxidase inhibitor sodium azide (NaN3) showed remarkable inhibitory effects on ROS generation induced by NP, but an inhibitor against mitochondrial respiratory function, (KCN), did not exhibit significant effect. The selective protein kinase C inhibitor Ro-32-0432, p38 MAP kinase inhibitor SB 203580, and ERK MAP kinase inhibitor PD 98059 also showed significant suppressive effects on NP-induced ROS generation. |
1(0,0,0,1) | Details |
| 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. Our laboratory has demonstrated that AMphis exposed to sodium azide display enhanced phagocytosis of P. aeruginosa. |
1(0,0,0,1) | Details |
| 7583793 | Jackola DR, Hallgren HM: Diminished cell-cell binding by lymphocytes from healthy, elderly humans: evidence for altered activation of LFA-1 function with age. J Gerontol A Biol Sci Med Sci. 1995 Nov;50(6):B368-77. In all cases, aggregation of cells began immediately upon addition of the protein kinase C activator phorbol (PMA) or the ionophore ionomycin, and continued until reaching an asymptotic limit by 20 minutes or less. Further, aggregation was Ca2+/Mg2+ dependent, and the reaction required metabolically active cells, as the reaction was inhibited by the addition of sodium azide and 2-deoxy- in both donor groups. |
1(0,0,0,1) | Details |
| 7894203 | Sandstrom PA, Chow DA: Phorbol ester tumor promoter regulation of natural antitumor antibody binding depends on protein kinase C and an intact microfilament system. Nat Immun. 1994 Nov-Dec;13(6):331-43. Colchicine, cytochalasin B and sodium azide inhibited the NAb binding of TPA-treated cells, while only colchicine reduced the binding of controls, suggesting the dependence of the TPA-induced increase in NAb binding on microfilament organization and active energy production. |
1(0,0,0,1) | Details |
| 9780311 | Aten RF, Kolodecik TR, Rossi MJ, Debusscher C, Behrman HR: treatment in vivo, but not in vitro, stimulates protein kinase C-activated production by nonsteroidogenic cells of the rat corpus luteum. Biol Reprod. 1998 Nov;59(5):1069-76. In conclusion, there is a generator in luteinized ovaries that is activated through a protein kinase C pathway, localized in nonsteroidogenic cells, transiently increased during PGF2alpha-induced luteolysis in vivo, and elevated during natural luteal regression. The response to TPA and zymosan was inhibited by the /-oxidase inhibitor, diphenylene iodonium (ID50 = 5 microM for TPA), but not by the mitochondrial inhibitors, rotenone, or sodium azide. |
1(0,0,0,1) | Details |
| 10579466 | Orie NN, Zidek W, Tepel M: and /calmodulin kinases are common signaling components in the generation of reactive species in human lymphocytes. Life Sci. 1999;65(20):2135-42. These increases were significantly inhibited by catalase, sodium azide, and dimethylsulfoxide but not by superoxide dismutase, suggesting that the ROS apparently included peroxide, singlet and but not PMA-induced responses were reduced by tyrphostin (p <0.01), ST-638 (p <0.05), KN-62 (p <0.001), bisindolylmaleimide (p <0.001), RO-31-8220 (p <0.001), and by LY-83583 (p <0.001), suggesting significant involvement of kinase, /calmodulin kinase II, protein kinase C and guanylyl cyclase. fMLP-induced responses were significantly reduced by only tyrphostin (p <0.001), ST-638 (p <0.05), and KN-62 (p <0.01). |
1(0,0,0,1) | Details |
| 17900002 | Okai Y, Sato EF, Higashi-Okai K, Inoue M: Potentiating effect of an endocrine disruptor, paranonylphenol, on the generation of reactive species (ROS) in human venous blood -- association with the activation of signal transduction pathway. J UOEH. 2007 Sep 1;29(3):221-33. An -dependent oxidase inhibitor, diphenyl iodonium (DPI), and a myeloperoxidase inhibitor, sodium azide (NaN3), showed remarkable inhibitory effects on ROS generation induced by NP, but an inhibitor against mitochondrial respiratory function, (KCN), did not exhibit a significant effect. Selective protein kinase C inhibitor, Ro-32-0432, p38 MAP kinase inhibitor, SB-203580, and ERK MAP kinase inhibitor, PD 98059, showed significant suppressive effects on NP-induced ROS generation. |
1(0,0,0,1) | Details |
| 7531437 | Berridge MV, Tan AS: Interleukin-3 facilitates transport in a myeloid cell line by regulating the affinity of the transporter for involvement of protein phosphorylation in transporter activation. Biochem J. 1995 Feb 1;305 ( Pt 3):843-51. The light-activated protein kinase C inhibitor, calphostin C, also inhibited control and IL-3-stimulated transport but without preference for IL-3 responses. Inhibition of DNA synthesis with mitomycin C or with the respiratory poison, sodium azide, did not affect the ability of IL-3 to promote transport. |
1(0,0,0,1) | Details |
| 10926312 | Orie NN, Zidek W, Tepel M: Increased intracellular generation of reactive species in mononuclear leukocytes from patients with diabetes mellitus type 2. Exp Clin Endocrinol Diabetes. 2000;108(3):175-80. Measurements were made in the presence or absence of superoxide dismutase, sodium azide, or bisindolylmaleimide 1. The formyl-Met---induced responses were significantly inhibited by and bisindolylmaleimide 1 (p <0.01), suggesting the involvement of kinase and protein kinase C. |
1(0,0,0,1) | Details |
| 10601426 | Tanabe M, Mori M, Gahwiler BH, Gerber U: Apamin-sensitive conductance mediates the K (+) current response during chemical ischemia in CA3 pyramidal cells. J Neurophysiol. 1999 Dec;82(6):2876-82. Experiments with charybdotoxin (10 nM) and tetraethylammonium (TEA; 1 mM), or with the protein kinase C activator, phorbol 12,13- (PDAc; 3 microM), ruled out an involvement of a large conductance-type or an apamin-insensitive small conductance, respectively. |
1(0,0,0,1) | Details |
| 11547566 | Nakano H, Gasparro FP, Uitto J: UVA-340 as energy source, mimicking natural sunlight, activates the transcription factor AP-1 in cultured fibroblasts: evidence for involvement of protein kinase-C. Photochem Photobiol. 2001 Aug;74(2):274-82. Free radical quenchers, sodium azide and did not affect the AP-1 binding activity. |
1(0,0,0,1) | Details |
| 11354246 | Hedin HL, Nilsson L, Fowler CJ: Effects of staurosporine, U-73122, wortmannin, and sodium azide upon the release of secreted beta-amyloid precursor protein from human platelets in response to thrombin stimulation. Mol Cell Biochem. 2001 Mar;219(1-2):145-52. |
0(0,0,0,0) | Details |
| 8923488 | Kawai N, McCarron RM, Spatz M: Na (+)-K (+)-Cl- cotransport system in brain capillary endothelial cells: response to endothelin and hypoxia. Neurochem Res. 1996 Oct;21(10):1259-66. Oligomycin, sodium azide, or antimycin A increased Na (+)-K (+)-Cl- cotransport activity by 80-200%. |
0(0,0,0,0) | Details |