|1.||Banik, Naren L: 28 articles (10/2015 - 06/2002)|
|2.||Ray, Swapan K: 25 articles (11/2012 - 06/2002)|
|3.||Azuma, Mitsuyoshi: 16 articles (09/2015 - 02/2002)|
|4.||Wang, Kevin K W: 15 articles (09/2014 - 12/2005)|
|5.||Shearer, Thomas R: 14 articles (09/2015 - 02/2002)|
|6.||Saido, Takaomi C: 14 articles (01/2015 - 01/2003)|
|7.||Sorimachi, Hiroyuki: 14 articles (08/2013 - 07/2003)|
|8.||Banik, N L: 13 articles (09/2009 - 01/2000)|
|9.||Greer, Peter A: 12 articles (01/2016 - 06/2006)|
|10.||Hayes, Ronald L: 12 articles (03/2014 - 01/2004)|
08/01/2010 - "We investigated the regulation and time-course of calpain activation secondary to transient ischemia and the efficacy of its inhibition at reperfusion as a therapeutic strategy to limit infarct size. "
07/26/2014 - "Numerous experimental studies reveal an essential role of the calpain system in myocardial injury during ischemia, reperfusion and postischemic structural remodelling. "
07/01/2011 - "The aim of the study was to investigate how PLB is dephosphorylated in ischemia and to determine whether PLB dephosphorylation causes myocardial hypercontraction and calpain activation through Ca(2+) overload in reperfusion. "
04/01/2007 - "Our study further indicates that accumulation of p35 and its calpain-mediated cleavage product, p25 may account for the deregulation of Cdk5 induced by transient ischemia. "
12/01/2003 - "In the present study, we investigated the activity and expression of CaN and the effect of calpain in rat heart after ischemia and reperfusion. "
|2.||Brain Injuries (Brain Injury)
12/14/2005 - "In this study, we evaluated caspase- and calpain-mediated mechanisms of cell death of neonatal mouse C17.2 progenitor cells, transplanted at 24 h following lateral fluid percussion brain injury (FP) in rats. "
11/15/2013 - "Collectively, opening of the astrocytic Cx43-HC and neuronal Cx36-HC would induce the regional spread of cortical neuronal death through μ-calpain activation in the rat brain injury model."
12/01/2012 - "Calpain expression in the brain cortex after traumatic brain injury."
09/01/2012 - "The calpain family has a well-established causal role in neuronal cell death following acute brain injury: their activation has been observed to progressively increase after either contusive or diffuse brain trauma in animals, suggesting calpain to be a mediator of early neuronal damage. "
06/01/2012 - "Although enhanced calpain activity is well documented after traumatic brain injury (TBI), the pathways targeting specific substrate proteolysis are less defined. "
05/01/2015 - "This study investigated whether calpain activation causes ER stress, thereby mediating cardiomyocyte apoptosis in an in vitro model of hypoxia/re-oxygenation (H/R). "
08/15/1995 - "The increase in calpain activity during hypoxia and the inhibitor studies with CBZ therefore supported a role for calpain as a mediator of hypoxia-induced proximal tubular injury."
01/01/2015 - "Hypoxia induces calpain activity and degrades SMAD2 to attenuate TGFβ signaling in macrophages."
04/01/2014 - "In cultured human retina, hypoxia caused activation of calpain and subsequent proteolysis of critical substrates. "
04/01/2014 - "Calpain protease causes hypoxia-induced proteolysis in cultured human retina."
03/01/2011 - "Further studies will be required concerning the other members of the calpain family and their potential implication in cancer development before considering treatments targeting their activity."
01/01/2011 - "Additional studies including more patients are required to elucidate the functional role and impact of calpain in tumors in detail."
05/15/2010 - "One of the major results of this study is the positive linear correlation between calpain activity and migration velocity presenting calpains as a marker of tumor aggressiveness. "
10/01/2007 - "The calpain inhibition studies suggest that inhibiting this activity may be a potential treatment for some androgen-independent prostate tumors."
09/25/1995 - "Our study thus suggests that calpain-like activity may be a potentially therapeutic target for cancer."
10/01/2014 - "In conclusion, although JNK and calpain both contribute to PARP1-induced necrosis, they do so via parallel mechanisms. "
10/01/2014 - "In contrast, inhibition of calpain either by Ca(2+) chelation or knockdown attenuated necrosis, but did not affect JNK activation or AIF translocation. "
10/01/2014 - "PARP1-mediated necrosis is dependent on parallel JNK and Ca²⁺/calpain pathways."
01/01/2014 - "This necrosis was dependent upon the Ca(2+) activated protease calpain, as pharmacologic inhibition prevented this secondary necrosis. "
06/01/2013 - "At 24 h after SE, activity of calpain I, neuronal necrosis and apoptosis increased in the hippocampus. "
|2.||Caspase 3 (Caspase-3)
|5.||Proteins (Proteins, Gene)
|6.||calpain inhibitor III
|8.||Cysteine Proteases (Cysteine Protease)
|9.||Proteasome Endopeptidase Complex (Proteasome)
|2.||Drug Therapy (Chemotherapy)
|4.||Protein-Restricted Diet (Diet, Protein Restricted)
|5.||Mechanical Ventilators (Ventilator)