|1.||Lee, Chung Soo: 18 articles (08/2015 - 10/2009)|
|2.||Kim, Yun Jeong: 13 articles (12/2014 - 10/2009)|
|3.||Chen, Qun: 10 articles (11/2014 - 07/2004)|
|4.||Chan, Pak H: 10 articles (04/2012 - 01/2002)|
|5.||Steinberg, Gary K: 10 articles (09/2007 - 01/2002)|
|6.||Borutaite, Vilmante: 9 articles (01/2015 - 04/2003)|
|7.||Lesnefsky, Edward J: 9 articles (11/2014 - 07/2004)|
|8.||Sapolsky, Robert M: 9 articles (01/2010 - 05/2003)|
|9.||Kim, Wonyong: 8 articles (11/2012 - 04/2010)|
|10.||Myung, Soon Chul: 8 articles (11/2012 - 04/2010)|
10/01/2002 - "Results showed that ischemic preconditioning induced by a 3-min ischemic episode dramatically reduced the loss of hippocampal CA1 neurons resulting from a subsequent 8-min ischemia 7 days after reperfusion, and this protection was associated with a preservation of mitochondrial cytochrome c as examined after early reperfusion. "
05/01/1999 - "Cytosolic cytochrome c was detected as early as 1 hr after ischemia, and correspondingly, mitochondrial cytochrome c showed a significant reduction 2 hr after ischemia (p < 0.01). "
05/15/2007 - "By histological examinations and cytochrome c release assessments, the protective effects of these drugs on the DND of hippocampal CA1 neurons in mice subjected to transient ischemia were examined. "
01/01/2014 - "Addition of exogenous cytochrome c to mitochondria isolated from ischemia brains had no effect on respiration in all models used in this study. "
04/25/2010 - "The present study aimed to investigate the change of cytochrome c in postconditioning-attenuated ischemia-reperfusion (I/R)-induced mucosal apoptosis in rat intestine compared with ischemic preconditioning (IPC). "
03/01/2009 - "This study aimed to evaluate serum cytochrome c (cyto-c) levels as a novel role of tumor marker in patients with operable malignant tumors. "
12/01/2006 - "One of these studies concluded that in some tissues apoptosis may require Apaf-1 but not cytochrome c, which indicated the need to analyze the requirement of cytochrome c beyond the mouse models, and in human tumor cells in particular. "
12/01/2002 - "This study suggests that the combination of Act D-induced down-regulation of XIAP (Signal I) and Apo2L/TRAIL-induced release of cytochrome c (Signal II) leads to the reversal of resistance to Apo2L/TRAIL-mediated apoptosis in the tumor cells. "
11/05/2001 - "This study demonstrates that GrB-cleaved Bid, which differs in size and site of cleavage from caspase-8-cleaved Bid, utilizes Bak for cytochrome c release, and therefore, suggests that deficiency in Bak may serve as a mechanism of immune evasion for tumor or viral infected cells."
11/01/2015 - "Further investigations disclosed that TB1 trigger apoptosis by activating the mitochondria-cytochrome c-caspase apoptotic pathway, it also exhibited the anti-migratory effect on cancer cells. "
|3.||Brain Ischemia (Cerebral Ischemia)
11/01/1998 - "The present study examined the expression of cytochrome c protein after transient focal cerebral ischemia in rats, in which apoptosis was assumed to contribute to the expansion of the ischemic lesion. "
01/23/2015 - "There was no loss of mitochondrial cytochrome c during 30-120 min of brain ischemia. "
02/22/2013 - "These results suggest that mdivi-1 exerts neuroprotective effects against nerve injury after cerebral ischemia/reperfusion, and the underlying mechanism may be through the prevention of Cytochrome C release and suppression of the mitochondrial apoptosis pathway."
01/01/2011 - "The release of cytochrome c from the mitochondria following cerebral ischemia is a key event leading to cell death. "
12/29/2010 - "MLCDP treatment when compared to free or LCDP treatment prevented global moderate cerebral ischemia-reperfusion induced mitochondrial damage as evident ultra structurally and release of cytochrome c (cyt c) from mitochondria into cytosol and protected mitochondria to restore its normal structure and functions."
05/15/2003 - "Mitochondrial permeability transition and cytochrome c release in ischemia-reperfusion injury of the rat liver."
01/01/2003 - "We studied the timing of cytochrome c release during I/R and whether subsequent caspase activation contributes to reperfusion injury in confluent chick cardiomyocytes. "
11/15/2010 - "Patients with clinical signs of myocardial reperfusion injury had a significantly greater cytochrome c peak value than patients without reperfusion injury (median 1.65 ng/ml, interquartile range 1.20 to 2.20, vs 1.1 ng/ml, interquartile range 0.65 to 1.55; p = 0.04). "
11/17/2014 - "To further assess the effects of GA on cerebral ischemia/reperfusion injury, 2, 3, 5-triphenyl-tetrazolium chloride (TTC) staining, dUTP nick-end labeling (TUNEL) assay, and Cytochrome C (Cyt C) release were performed in MCAO rats. "
02/22/2013 - "Mdivi-1 treatment blocked apoptotic cell death in cerebral ischemia/reperfusion injury, and significantly decreased the expression of Drp1 and Cytochrome C. "
06/01/2005 - "Recent studies demonstrate that hypoxia/reoxygenation can activate death receptor and mitochondria-dependent apoptotic pathways, involving Bid and Bax mitochondrial translocation and cytochrome c release. "
02/13/2004 - "Recent studies have shown that hypoxia/reoxygenation can induce Bax translocation and cytochrome c release. "
06/15/1953 - "[Study on the action of cytochrome C on experimental anoxia in isolated head of dog]."
11/15/2015 - "Under mild hypoxia, the steep slope of oxidation of cytochrome c when flux remains more stable represents a cushioning mechanism that helps to maintain respiration high at the onset of hypoxia. "
04/06/2015 - "Increased levels of reduced cytochrome c in ex vivo cells are also observed during hypoxia and reoxygenation by Raman microspectroscopy. "
|1.||Caspase 3 (Caspase-3)
|2.||Reactive Oxygen Species (Oxygen Radicals)
|4.||Adenosine Triphosphate (ATP)
|5.||Caspase 8 (Caspase-8)
|8.||Proteins (Proteins, Gene)
|10.||Apoptosis Inducing Factor
|2.||Total Parenteral Nutrition
|5.||Drug Therapy (Chemotherapy)