|1.||Anderson, Mark E: 42 articles (01/2016 - 09/2002)|
|2.||Maier, Lars S: 28 articles (07/2015 - 05/2003)|
|3.||Bers, Donald M: 22 articles (05/2015 - 05/2003)|
|4.||Mohler, Peter J: 20 articles (07/2015 - 09/2007)|
|5.||Backs, Johannes: 18 articles (12/2015 - 07/2006)|
|6.||Brown, Joan Heller: 17 articles (12/2014 - 01/2002)|
|7.||Mattiazzi, Alicia: 15 articles (01/2016 - 01/2002)|
|8.||Hund, Thomas J: 14 articles (07/2015 - 09/2008)|
|9.||Fukunaga, Kohji: 13 articles (10/2015 - 09/2002)|
|10.||Colbran, Roger J: 11 articles (04/2015 - 09/2002)|
|1.||Cardiovascular Diseases (Cardiovascular Disease)
01/01/2014 - "Indeed, improved understanding of CaMKII activation mechanisms could potentially lead to new clinical therapies for the treatment or prevention of cardiovascular disease. "
01/01/2015 - "Regulation of CaMKII signaling in cardiovascular disease."
02/01/2014 - "[Recent progress of Ca2+/calmodulin-dependent protein kinase II in cardiovascular diseases]."
07/01/2011 - "Here we review roles of CaMKII in cardiovascular disease with an eye to understanding how CaMKII may act as a transduction signal to connect pro-oxidant conditions into specific downstream pathological effects that are relevant to rare and common forms of cardiovascular disease."
12/01/2009 - "These unexpected new data identify an alternative activation pathway for CaMKII in common cardiovascular disease. "
07/07/2008 - "In the present study we investigated the effects of global ischemia followed by reperfusion and of SE on the phosphorylation of CaMKII on T253 in rat forebrains and compared this to the phosphorylation of T286. "
03/01/2007 - "The goal of the present study is to investigate the role of CaMKII in irreversible ischemia and reperfusion (I/R) injury. "
04/01/2015 - "CaMKII expression was not changed in ventricular tissues, although CaMKIIδ activation and phosphorylation of downstream targets was enhanced in ArKO hearts subjected to ischemia-reperfusion. "
02/15/2015 - "In ischemia/reperfusion, female hearts (vs male) exhibited less arrhythmias (59 ± 18 vs 548 ± 9, s, p<0.05), yet had augmented P-CaMKII (2.69 ± 0.30 vs 1.50 ± 0.14, rel. "
01/01/2014 - "This review summarizes the current experimentally derived understanding of CaMKII participation in mediating the pathophysiology of the heart in ischemia and in reperfusion, and highlights priority future research directions. "
03/01/2011 - "These results demonstrate that the phosphorylation of CaMKII and GluR1 occurs downstream of the Tyr1472 phosphorylation of NR2B subunits in the spinal cord and give the first suggestion that activation of CaMKII and GluR1-AMPA receptors may be involved in mechanical allodynia caused by peripheral nerve injury."
01/06/2010 - "Ca2+/calmodulin-dependent protein kinase II alpha is required for the initiation and maintenance of opioid-induced hyperalgesia."
01/01/2009 - "By contrast, a CaMKII inhibitor prevented the development and expression of nerve injury-induced tactile allodynia and reduced both the level of cPLA2 phosphorylation and the number of DRG neurons showing translocated cPLA2 in response to nerve injury. "
02/01/2008 - "Our findings suggest that a CaMKII-dependent NO/sGC/PKG pathway is involved in the RS-induced SRP, which has pathological relevance to hyperalgesia and allodynia."
01/01/2006 - "Here we show that genetic overexpression of CaMKII in the mouse forebrain selectively inhibits tissue injury-induced behavioral sensitization, including allodynia and hyperalgesia, while behavioral responses to acute noxious stimuli remain intact. "
01/03/2014 - "The aim of this study was to test whether intraganglionic (i.g.) injection of CaMKII inhibitors may alleviate pain-related behavior in diabetic rats. "
10/21/2015 - "Loss of CaMKII function, such as occurred in rats during sensory deprivation, elevated the generation and propagation of impulses by LTMRs, and altered the spinal cord circuitry in such a way that low-threshold mechanical stimuli produced pain behavior. "
10/21/2015 - "We conclude that, without normal sensory activity to maintain adequate levels of CaMKII function, the touch pathway shifts into a pain system. "
10/21/2015 - "Together, these consequences of reduced CaMKII function in Aβ-LTMRs cause low-intensity mechanical stimulation to produce pain behavior. "
08/06/2015 - "Thus, loss of CaMKII signaling in sensory neurons after peripheral nerve injury may contribute to neuronal dysfunction and pain."
|5.||Alzheimer Disease (Alzheimer's Disease)
02/01/2015 - "CaMKII-dependent dendrite ramification and spine generation promote spatial training-induced memory improvement in a rat model of sporadic Alzheimer's disease."
10/01/2015 - "Ribosylation triggering Alzheimer's disease-like Tau hyperphosphorylation via activation of CaMKII."
11/07/2005 - "Reduction of NR1 and phosphorylated Ca2+/calmodulin-dependent protein kinase II levels in Alzheimer's disease."
12/26/2003 - "These results suggested that CaMKII is involved in the phosphorylation of tau in Alzheimer's disease brain."
09/19/1994 - "These results suggest CaM kinase II expression in the Alzheimer's disease brain is unaltered despite marked neuropathological changes."
|1.||Calcium-Calmodulin-Dependent Protein Kinase Type 2
|2.||Brain-Derived Neurotrophic Factor (BDNF)
|4.||Calmodulin (Calcium-Dependent Activator Protein)
|5.||Calcium-Calmodulin-Dependent Protein Kinases
|8.||AMPA Receptors (AMPA Receptor)