| Name | protein kinase C (protein family or complex) |
|---|---|
| Synonyms | Protein kinase C; PKC |
| Name | piperazine |
|---|---|
| CAS | piperazine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 12663510 | Zhang J, Svehlikova V, Bao Y, Howie AF, Beckett GJ, Williamson G: Synergy between and in the induction of thioredoxin reductase 1 requires both transcriptional and translational modulation. Carcinogenesis. 2003 Mar;24(3):497-503. Modulation of TrxR1 mRNA by was and protein kinase C-dependent, as L-buthionine-S,R-sulfoximine (a specific inhibitor of synthesis), and the protein kinase C inhibitor 1-(5-isoquinolinesulfonyl)-2-methyl-piperazine, significantly reduced the induction. |
81(1,1,1,1) | Details |
| 12167288 | Vidulescu C, Mironneau J, Mironneau C, Popescu LM: Messenger molecules of the phospholipase signaling system have dual effects on vascular smooth muscle contraction. J Cell Mol Med. 2000 Jul-Sep;4(3):196-206. However, when added during -induced plateau, phospholipase D shortly potentiated it. b) The protein kinase C activator, phorbol dibutyrate potentiated both the exogenous phospholipase C-induced contraction and the -induced plateau, while the protein kinase C inhibitor 1-(-5-isoquinolinesulfonyl)-2-methyl-piperazine relaxed the plateau. c) When added before indomethacin inhibited both phasic and tonic contractions, but when added during the tonic contraction shortly potentiated it. |
32(0,1,1,2) | Details |
| 11780430 | Yang X, Hui J, Jiang W: Angiotensin II type 1 receptor modulation of L-type currents in guinea-pig ventricular cells. Chin Med J. 2001 Jun;114(6):577-82. OBJECTIVE: To study the cellular mechanism of the effect of Ang II on ICa,L in single guinea-pig ventricular cells by using losartan and 1-(5-lsoquinolinylsulfonyl)-2-Methyl-Piperazine (H-7) as the Ang II type 1 receptor (AT1) inhibitor and protein kinase C inhibitor, respectively. |
32(0,1,1,2) | Details |
| 11747364 | Rieck PW, Cholidis S, Hartmann C: Intracellular signaling pathway of FGF-2-modulated corneal endothelial cell migration during wound healing in vitro. Exp Eye Res. 2001 Nov;73(5):639-50. In this study, it has been attempted to identify elements of the intracellular signaling pathway activated through basic Fibroblast Growth Factor (FGF-2)- and Protein Kinase C (PKC)-modulated migration, using specific inhibitors and stimulators of second messengers in a cell culture model. In different experiments, cells were incubated with either FGF-2 (10 ng ml (-1)), pertussis toxin (PTX; 1-50 ng ml (-1)), phorbol 12- 13- (PMA; 50 ng ml (-1)), 2,4'-di-bromoacetophenone (DAP; 5 microM), 1-(5-iosquinolinesulphonyl)-2-methyl-piperazine dihydrochloride (H7; 10 microM), indomethacin (5 ng ml (-1)), nordihydroguaiaretic acid (NDGA; 10 ng ml (-1)), 2-(4-morpholinyl)-8-pheny-4H-1-benzopyran-4-one (LY294002; 10 microM) or different combinations of these agents. |
2(0,0,0,2) | Details |
| 19654408 | Zarrinkar PP, Gunawardane RN, Cramer MD, Gardner MF, Brigham D, Belli B, Karaman MW, Pratz KW, Pallares G, Chao Q, Sprankle KG, Patel HK, Levis M, Armstrong RC, James J, Bhagwat SS: AC220 is a uniquely potent and selective inhibitor of FLT3 for the treatment of acute myeloid leukemia (AML). Blood. 2009 Oct 1;114(14):2984-92. Epub 2009 Aug 4. We report the characterization of AC220, a second-generation FLT3 inhibitor, and a comparison of AC220 with the first-generation FLT3 inhibitors CEP-701, MLN-518, PKC-412, sorafenib, and sunitinib. |
1(0,0,0,1) | Details |
| 16682960 | Kim HW, Kwon YB, Roh DH, Yoon SY, Han HJ, Kim KW, Beitz AJ, Lee JH: Intrathecal treatment with sigma1 receptor antagonists reduces formalin-induced phosphorylation of NMDA receptor subunit 1 and the second phase of formalin test in mice. Br J Pharmacol. 2006 Jun;148(4):490-8. Epub 2006 May 8. I.t. injection of BD-1047 also reduced formalin-evoked Fos expression and pNR1 at the protein kinase C-dependent site, serine-896 (Ser896) and the protein kinase A-dependent site, serine-897 (Ser897) in spinal dorsal horn.i.t. |
1(0,0,0,1) | Details |
| 12788814 | Fahrmann M, Kaufhold M, Pfeiffer AF, Seidler U: Protein kinase C-alpha attenuates cholinergically stimulated gastric acid secretion of rabbit parietal cells. Br J Pharmacol. 2003 Jun;139(3):545-54. (1) The phorbolester 12-O-tetradecanoyl phorbol-13- (TPA), an activator of protein kinase C (PKC), inhibits cholinergic stimulation of gastric acid secretion. PKC-alpha represents the only -dependent PKC isoenzyme that has been detected in rabbit parietal cells. (3) Go 6976, an inhibitor of -dependent PKC, concentration-dependently antagonized the inhibitory effect of TPA, and, therefore, revealed the action of PKC-alpha on carbachol-induced acid secretion in rabbit parietal cells. (4) TPA exerted no additive inhibition of carbachol-stimulated acid secretion if acid secretion was partially inhibited by the potent CaMKII inhibitor 1-[N,O-bis (5-isoquinolinsulfonyl)-N-methyl-L-tyrosyl]-4-phenyl-piperazine (KN-62). (5) Since both kinase modulators, TPA and KN-62, affected no divergent signal transduction pathways in the parietal cell, an in vitro model has been used to study if PKC directly targets CaMKII. |
1(0,0,0,1) | Details |
| 15456534 | Zhang XF, Guo SZ, Lu KH, Li HY, Li XD, Zhang LX, Yang L: Different roles of PKC and PKA in effect of interferon-gamma on proliferation and collagen synthesis of fibroblasts. Acta Pharmacol Sin. 2004 Oct;25(10):1320-6. The proliferation and collagen synthesis were enhanced by PKC activator (containing diacylglycerol and Ca2+) and PKA inhibitor [H (7) 250 micromol/L, 1-(5-isoquinolinylsulfonyl)-2-methyl piperazine], and inhibited by PKC inhibitor (GF109 250 micromol/L) and PKA activator (cAMP 25 micromol/L) (P <0.01). AIM: To study the signal roles of protein kinase C (PKC) and protein kinase A (PKA) in the influence of interferon-gamma (IFN-gamma) on proliferation and collagen synthesis of fibroblasts derived from hypertrophic scar (HS-FB) and normal skin (NS-FB). |
1(0,0,0,1) | Details |
| 11730364 | Biswas SK, Sodhi A, Paul S: Regulation of production by murine peritoneal macrophages treated in vitro with chemokine monocyte chemoattractant protein 1. Nitric Oxide. 2001 Dec;5(6):566-79. Investigating the signal transduction pathway responsible for the NO production by the MCP-1-activated murine peritoneal macrophages, it was observed that the pharmacological inhibitors wortmannin, H-7 (1-(5-isoquinoline sulfonyl)-2-methyl piperazine dihydrochloride), and PD98059 blocked the MCP-1-induced NO production, suggesting the probable involvement of phosphoinositol-3-kinase, protein kinase C, and p42/44 MAPkinases in the above process. |
0(0,0,0,0) | Details |
| 11498991 | Zhu FM, Wen ZB, He XF, Li JC, He SL: [Expression of tissue factor of astrocytes and its signal transductional pathways]. Sheng Li Xue Bao. 1999 Jun;51(3):291-6. The results showed that 4-bromo ionophore (A23187) and phorbol 12- 13- (PMA) enhanced significantly the TF expression of astrocytes, but the expression was decreased markedly by trifluoperazine (TFP) and 1-(5-isoquinolinyl sulfonyl)-3-methyl-piperazine (H7) in the basic medium. The results above indicate that astrocytes can express TF activity in the basic medium, which is promoted by thrombin, probably through some pathways involving Ca2+/CaM and protein kinase C (PKC). |
1(0,0,0,1) | Details |