|1.||Xu, Jing: 5 articles (06/2011 - 01/2008)|
|2.||Li, Tao: 5 articles (06/2011 - 01/2008)|
|3.||Yang, Guangming: 4 articles (06/2011 - 01/2008)|
|4.||Liu, Liangming: 4 articles (06/2011 - 01/2008)|
|5.||Fisher, Steven A: 3 articles (05/2015 - 05/2004)|
|6.||Ming, Jia: 3 articles (06/2010 - 01/2008)|
|7.||Ng, Irene Oi-Lin: 2 articles (01/2013 - 05/2009)|
|8.||Wong, Carmen Chak-Lui: 2 articles (01/2013 - 05/2009)|
|9.||Tung, Edmund Kwok-Kwan: 2 articles (01/2013 - 05/2009)|
|10.||Fortin, Samuel: 2 articles (07/2012 - 08/2011)|
|1.||Muscle Spasticity (Spastic)
03/21/2000 - "These results indicate that Rho-kinase is upregulated at the spastic site and plays a key role in inducing vascular smooth muscle hypercontraction by inhibiting myosin phosphatase through the phosphorylation of MBS in our porcine model."
02/01/2005 - "In animal models with coronary spasm Rho-kinase is upregulated at the spastic site and plays a key role in inducing vascular smooth muscle hypercontraction by inhibiting myosin light chain phosphatase, resulting in enhancement of its phosphorylation. "
03/21/2000 - "Western blot analysis showed that during the serotonin-induced contractions, the extent of phosphorylation of the myosin-binding subunit of myosin phosphatase (MBS), one of the major substrates of Rho-kinase, was significantly greater in the spastic than in the control segment and that the increase in MBS phosphorylations was also markedly inhibited by Y-27632. "
02/08/2008 - "Administration of fasudil twice daily was continued until day 4. Fasudil prevented the accumulation of neutrophils within the brain as seen from measurements taken on day 3, and improved neuronal functions and reduced the infarction area as seen on day 5. Fasudil and hydroxyfasudil, an active metabolite of fasudil, concentration-dependently inhibited phosphorylation of myosin binding subunit of myosin phosphatase in neutrophils. "
06/01/2009 - "MYPT1, the targeting subunit of smooth-muscle myosin phosphatase, is a substrate for the asparaginyl hydroxylase factor inhibiting hypoxia-inducible factor (FIH)."
08/01/2014 - "The augmentation of contraction caused by hypoxia or cIMP was accompanied by increased phosphorylation of myosin phosphatase target subunit 1 at Thr(853), which was prevented by the ROCK inhibitor Y-27632. "
01/01/2010 - "In hypoxia-treated vascular smooth muscle cells (VSMCs), the effects of PKC-alpha and PKC-epsilon agonists on protein expression and activity of CPI-17 and ZIPK and the modulating effects of CPI-17 and ZIPK on the regulation of PKC-alpha and PKC-epsilon on the activity of myosin light chain phosphatase (MLCP) were observed. "
12/01/2008 - "Auto-phosphorylation of srcFKs and phosphorylation of the regulatory subunit of myosin phosphatase (MYPT-1) and myosin light-chain (MLC(20)) in response to hypoxia were determined by western blotting. "
10/01/2003 - "Hypoxia inhibits myosin phosphatase in pulmonary arterial smooth muscle cells: role of Rho-kinase."
05/11/2007 - "In the present study, we hypothesized that heat shock augments myosin phosphatase target-subunit (MYPT1) phosphorylation resulting in augmented vascular contraction. "
05/11/2007 - "Heat shock augments myosin phosphatase target-subunit phosphorylation."
06/01/2011 - "We used isolated superior mesenteric arteries (SMAs) from hemorrhagic-shock rats and hypoxia-treated vascular smooth muscle cells (VSMCs; mimicking the shock state) to observe the effects of platelet-derived growth factor (PDGF; Rac1 stimulator) and NSC23766 (Rac1 antagonist) on vascular reactivity and the relationship with the Rho kinase-myosin light-chain phosphatase (MLCP) and p21-activated kinase (PAK)-myosin light-chain kinase (MLCK) signal pathway. "
08/26/2011 - "The defective protein level of myosin light chain phosphatase (MLCP) in the isolated saphenous vein, as a vascular conduit in coronary artery bypass grafting (CABG), harvested from patients with diabetes mellitus (DM)."
01/01/2016 - "This study was designed to evaluate whether melatonin attenuates arteriosclerosis and endothelial permeability by suppressing the myosin light-chain kinase (MLCK)/myosin light-chain phosphorylation (p-MLC) system via the mitogen-activated protein kinase (MAPK) signaling pathway or by suppressing the myosin phosphatase-targeting subunit phosphorylation (p-MYPT)/p-MLC system in diabetes mellitus (DM). "
|4.||fasudil (AT 877)
|5.||Serotonin (5 Hydroxytryptamine)
|7.||Myosin Light Chains (Myosin Essential Light Chain)
|9.||Protein Kinase C
|1.||Coronary Artery Bypass (Coronary Artery Bypass Surgery)