|1.||Song, Bo: 3 articles (05/2004 - 10/2003)|
|2.||Collins, Steven J: 2 articles (11/2007 - 05/2007)|
|3.||Mueller, LeMoyne: 2 articles (11/2007 - 05/2007)|
|4.||Si, Jutong: 2 articles (11/2007 - 05/2007)|
|5.||Zhang, Guang-yi: 2 articles (05/2004 - 02/2004)|
|6.||Yan, Xue-bo: 2 articles (05/2004 - 02/2004)|
|7.||Meng, Fan-jie: 2 articles (05/2004 - 02/2004)|
|8.||Guo, Jun: 2 articles (02/2004 - 10/2003)|
|9.||Bränström, Robert: 1 article (01/2011)|
|10.||Farnebo, Lars-Ove: 1 article (01/2011)|
05/01/1999 - "Additional experiments showed that KN-62 also inhibited insulin- and hypoxia-stimulated transport by 37 and 40% respectively in isolated rat epitrochlearis (a fast-twitch muscle), indicating that the effect of KN-62 was not limited to the slow-twitch fibres of the soleus. "
01/01/2000 - "KN-62 did not alter sinus nerve activity and catecholamine release evoked by hypoxia, but this agent significantly reduced nerve activity and neurotransmitter release evoked by 100 microM nicotine. "
05/01/1999 - "Accordingly, KN-62 decreased the stimulated cell-surface GLUT4 labelling by a similar extent as the inhibition of glucose transport (insulin, 49% and hypoxia, 54%). "
10/01/2010 - "CaMKII Inhibitor KN-62 Blunts Tumor Response to Hypoxia by Inhibiting HIF-1α in Hepatoma Cells."
05/01/1995 - "Finally, KN-62 significantly reduced cellular calcium accumulation following either NMDA challenge or hypoxia/hypoglycemia insult. "
05/01/2004 - "However, the binding levels of both CaMKIIalpha with nNOS and Thr(286) autophosphorylated CaMKIIalpha with nNOS increased after ischemia, and were diminished by KN-62. "
05/01/2004 - "The distributions of nNOS were not affected by ischemia and KN-62. "
10/09/2003 - "Administrating KN-62 through cerebral ventricle (20 min before ischemia) not only remarkably decreased the binding of CaMK IIalpha to SynGAP but also attenuate the elevated serine phosphorylation of SynGAP following 20 min ischemia in hippocampus. "
05/01/2004 - "Serine phosphorylation of nNOS in P increased persistently during brain ischemia, and 15 min ischemia-induced serine phosphorylation of nNOS was attenuated significantly by KN-62. "
02/01/2004 - "The association-dissociation of PSD-95 and CaMKIIalpha to and from N-methyl-D-aspartate (NMDA) receptor induced by ischemia and reperfusion and the effects of 1-[N,O-bis-(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenyl-piperazine (KN-62, a selective inhibitor of CaMKII) on these protein interactions were investigated. "
|3.||Small Cell Lung Carcinoma (Small Cell Lung Cancer)
12/22/1995 - "Inhibition of voltage-gated Ca2+ channel activity in small cell lung carcinoma by the Ca2+/calmodulin-dependent protein kinase inhibitor KN-62 (1-[N,O-bis(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenylpiperaz ine) ."
03/08/1996 - "Expression of Ca2+/calmodulin-dependent protein kinase types II and IV, and reduced DNA synthesis due to the Ca2+/calmodulin-dependent protein kinase inhibitor KN-62 (1-[N,O-bis(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4-phenyl piperazine) in small cell lung carcinoma."
12/01/2005 - "Likewise, KN-62, but not KN-04, an inactive analog, suppressed slow increases in EPP amplitude and miniature EPP frequency during long tetanus. "
12/01/2005 - "KN-62, a blocker of Ca(2+)/calmoduline-activated protein kinase II (CaMKII), slightly reduced short tetanus-induced rises in [Ca2+]i, but markedly the slow waxing and waning rises produced by repetitive tetani in both normal and low Ca2+, high Mg2+ solutions. "
04/01/1998 - "Second, the setting of the molecular switch, by the delivery of a tetanus (100 Hz, 1 s) in the presence of a specific NMDA receptor antagonist (R)-2-amino-5-phosphonopentanoate (AP5), reduced the sensitivity of LTP to KN-62, such that at a concentration of 3 microM it no longer blocked induction (though at 10 microM it did). "
03/15/1990 - "We examined the effect of KN-62 on cultured PC12 D pheochromocytoma cells. "
05/15/1991 - "A selective Ca2+/calmodulin-dependent protein kinase II inhibitor, KN-62, inhibits the enhanced phosphorylation and the activation of tyrosine hydroxylase by 56 mM K+ in rat pheochromocytoma PC12h cells."
05/15/1991 - "Involvement of Ca2+/calmodulin-dependent protein kinase II (Ca2+/CaM-kinase II) on the phosphorylation of tyrosine hydroxylase (TH, EC.188.8.131.52) in rat pheochromocytoma, PC12h cells was examined using KN-62, 1-[N,O-Bis(5-isoquinolinsulfonyl)-N-methyl-L-tyrosyl]-4-phenylpipe razine, a selective inhibitor of Ca2+/CaM-kinase II. Both the enhanced phosphorylation of TH and the activated L-3,4-dihydroxyphenylalanine (DOPA) formation in the high K+ depolarization were inhibited by 10 microM KN-62. "
|1.||Calcium-Calmodulin-Dependent Protein Kinase Type 2
|3.||Staphylococcal Protein A (A, Protein)
|4.||N- (2- (4- bromocinnamylamino)ethyl)- 5- isoquinolinesulfonamide (h89)
|8.||protein kinase modulator
|9.||Calmodulin (Calcium-Dependent Activator Protein)