| Name | calmodulin |
|---|---|
| Synonyms | CALM; CAM; CALM 1; CALM 2; CALM 3; CALM1; CALM2; CALM3… |
| Name | piperazine |
|---|---|
| CAS | piperazine |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 11137708 | Aoyama M, Grabowski DR, Holmes KA, Rybicki LA, Bukowski RM, Ganapathi MK, Ganapathi R: Cell cycle phase specificity in the potentiation of etoposide-induced DNA damage and apoptosis by KN-62, an inhibitor of -calmodulin-dependent enzymes. Biochem Pharmacol. 2001 Jan 1;61(1):49-54. The cell cycle phase-dependent induction of DNA damage and apoptosis by etoposide (VP-16) and its modulation by 1-[N,O-bis (1, 5-isoquinolinesulfonyl)-N-methyl-l-tyrosyl]-4-piperazine (KN-62), an inhibitor of -calmodulin-dependent enzymes, were examined in sensitive (HL-60/S) and VP-16-resistant (HL-60/DOX0.05) HL-60 cells. |
82(1,1,1,2) | Details |
| 14769205 | Meng FJ, Guo J, Song B, Yan XB, Zhang GY: Competitive binding of postsynaptic density 95 and Ca2+-calmodulin dependent protein kinase II to N-methyl-D-aspartate receptor subunit 2B in rat brain. Acta Pharmacol Sin. 2004 Feb;25(2):176-80. |
2(0,0,0,2) | 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 |
| 15066904 | De Lorenzo S, Veggetti M, Muchnik S, Losavio A: Presynaptic inhibition of spontaneous release induced by at the mouse neuromuscular junction. Br J Pharmacol. 2004 May;142(1):113-24. Epub 2004 Apr 5. Neither N-(2 [p-bromocinnamylamino]-ethyl)-5-isoquinolinesulfonamide (H-89, a PKA inhibitor), nor 1-(5-isoquinolinesulfonyl)-2-methyl-piperazine (H-7, a PKC antagonist), nor phorbol 12- 13- (PHA, a PKC activator) modified CCPA-induced presynaptic inhibition, suggesting that these second messenger pathways are not involved. 4. The effect of CCPA was eliminated by the calmodulin antagonist N-(6-aminohexil)-5-chloro-1-naphthalenesulfonamide hydrochloride (W-7) and by ethylene glycol-bis (beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid-acetoxymethyl ester epsilon6TDelta-BM, which suggests that the action of CCPA to modulate L-type VDCCs may involve Ca (2+)-calmodulin. 5. |
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. We observed that this effect strongly correlated with the inhibition of Ca (2+)/calmodulin-dependent protein kinase II (CaMKII) activity in rabbit parietal cells. (2) The aim of this study was to specify the function of PKC-alpha in cholinergically stimulated H (+) 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 |