|1.||Koohmaraie, M: 3 articles (05/2004 - 06/2001)|
|2.||Lametsch, René: 2 articles (05/2010 - 09/2008)|
|3.||Lee, Yong Sup: 2 articles (03/2009 - 01/2009)|
|4.||Jin, Changbae: 2 articles (03/2009 - 01/2009)|
|5.||Nakanishi, Tamao: 2 articles (04/2008 - 12/2004)|
|6.||Inomata, Mitsushi: 2 articles (04/2008 - 02/2007)|
|7.||Ozaki, Yasuhiko: 2 articles (04/2008 - 12/2004)|
|8.||Ogasawara, Mayumi S: 2 articles (04/2008 - 12/2004)|
|9.||Geddes, James W: 2 articles (02/2008 - 12/2005)|
|10.||Garcia, Matthew: 2 articles (02/2008 - 12/2005)|
|1.||Brain Ischemia (Cerebral Ischemia)
07/01/2005 - "The present data indicate that mu-calpain proteolysis plays an important role in the chain of events following cerebral ischemia. "
09/01/2006 - "In this study, we investigated the effect of E64d, a mu-calpain and cathepsin B inhibitor, in the prevention of neuronal and endothelial apoptotic cell death after focal cerebral ischemia in rats. "
12/01/2007 - "Synergetic effects of caspase 3 and mu-calpain in XIAP-breakdown upon focal cerebral ischemia."
02/01/1999 - "In the preceding reports, we demonstrated mu-calpain activation and subsequent rupturing of the lysosomal membrane of postischemic CA1 neurons and also increase of enzyme activity of cathepsins B and L in monkeys undergoing a complete 20-min whole brain ischemia. "
09/01/1995 - "If active eIF-4E is required for translation of its own mRNA, degradation of this protein during ischemia, possibly by activated mu-calpain, could be a direct mechanism of irreversible neuronal injury, and the rate of proteolysis of eIF-4E could place an upper time limit on the maximal duration of global brain ischemia compatible with neurologic recovery."
10/15/1998 - "Excessive mu-calpain activation has been linked to several cellular pathologies including excitotoxicity and ischemia. "
03/19/2010 - "Here, we studied the molecular interaction between activated mu-calpain and the lysosomal Hsp70.1 in the monkey hippocampal CA1 neurons after the ischemia-reperfusion insult. "
12/01/2007 - "The two fragments produced seem to be related to caspase-3 and mu-calpain activities, which are massively enhanced in tissues challenged by ischemia. "
02/16/2007 - "mu-Calpain was activated and p120-catenin was degraded after 36 h of ischemia in differentiated SH-SY5Y cells. "
09/26/2006 - "Selective deletion of the NH2-terminal variable region of cardiac troponin T in ischemia reperfusion by myofibril-associated mu-calpain cleavage."
09/01/2008 - "In the present study the influence of oxidation on activity and autolysis of mu-calpain was examined. "
05/01/2010 - "A faster decrease in pH resulted in reduced level of mu-calpain activity and increased autolysis of the enzyme, and hence an earlier loss of activity due to activation of mu-calpain in muscles with a fast pH decline. "
09/01/2008 - "Disulfide bond within mu-calpain active site inhibits activity and autolysis."
10/15/2006 - "If the [Ca(2+)] is raised sufficiently for long enough to initiate substantial autolysis of mu-calpain, the Ca(2+) sensitivity of the proteolytic activity is greatly increased, and it remains active even at 300 nm Ca(2+), with activity only ceasing if the [Ca(2+)] is decreased to approximately 50 nm Ca(2+), close to the normal resting [Ca(2+)]. "
10/15/2006 - "[Ca(2+)] has to be raised to >/= 2 microm for >/= 1 min to initiate detectable autolysis of mu-calpain and to activate appreciable proteolytic activity. "
|4.||Brain Injuries (Brain Injury)
02/01/1998 - "The detection of a shift in mu-calpain activity to the total membrane fraction first occurred at 3 hours after traumatic brain injury and became maximal at 24 hours after traumatic brain injury. "
10/01/1996 - "Our results indicate that rapid and persistent mu-calpain activation plays an important role in cortical neuronal degeneration after traumatic brain injury. "
10/01/1996 - "mu-calpain activation and calpain-mediated cytoskeletal proteolysis following traumatic brain injury."
02/01/1998 - "Subcellular localization and duration of mu-calpain and m-calpain activity after traumatic brain injury in the rat: a casein zymography study."
01/01/2000 - "Casein zymogram assessment of mu-calpain and m-calpain activity after traumatic brain injury in the rat in vivo."
12/01/2004 - "Conversely, the active form of mu-calpain was not detected in normal cells, but was abundant after hypoxia. "
12/01/2004 - "The proform of mu-calpain was detected in the cytoplasm of normal cells, and displayed a substantial decrease after hypoxia. "
12/01/2004 - "Cleavage of integrin by mu-calpain during hypoxia in human endometrial cells."
09/01/1994 - "Glucocorticoid pretreatment (beta-methasone, 0.4 mg x kg-1 x day-1) for 7 days produced a decrease in the ratio of activated mu-calpain in all three fractions in nearly all samples before, during, and after hypoxia, compared with untreated animals. "
06/01/2004 - "The present study aimed to clarify the time-course of the activation of the mu-calpain, and the expression of c-Fos, c-Jun, HSP70 and HSP27 proteins following severe HI (2 h hypoxia) and their relationship with each other. "
|8.||Protein Isoforms (Isoforms)
|10.||HSP27 Heat-Shock Proteins