|1.||Chan, Francis Ka-Ming: 3 articles (05/2014 - 12/2003)|
|2.||Miller, Joan W: 3 articles (09/2012 - 12/2010)|
|3.||Murakami, Yusuke: 3 articles (09/2012 - 12/2010)|
|4.||Vavvas, Demetrios G: 3 articles (09/2012 - 12/2010)|
|5.||Bertin, John: 2 articles (05/2014 - 10/2013)|
|6.||Kaiser, William J: 2 articles (05/2014 - 10/2013)|
|7.||Gough, Peter J: 2 articles (05/2014 - 10/2013)|
|8.||Mocarski, Edward S: 2 articles (05/2014 - 10/2013)|
|9.||Hisatomi, Toshio: 2 articles (09/2012 - 12/2010)|
|10.||Liu, Zheng-Gang: 2 articles (04/2012 - 03/2003)|
02/10/2006 - "One protective mechanism is through degradation of receptor-interacting protein (RIP), a key mediator of "programmed" necrosis. "
06/01/2011 - "Recent studies have shown that, when caspase pathways are blocked, receptor interacting protein (RIP) kinases promote necrosis and overcome apoptosis inhibition. "
02/01/2015 - "Furthermore, we demonstrated that GOLPH3 promoted K63-linked polyubiquitination of tumour necrosis factor receptor-associated factor 2 (TRAF2), receptor interacting protein (RIP) and NF-κB essential modulator (NEMO) and substantially sustained the activation of NF-κB in HCC cells. "
01/01/2013 - "Necrosis, as apoptosis, is a regulated form of cell death, and Poly-(ADP-Ribose) Polymerase-1 (PARP-1) and Receptor-Interacting Protein (RIP) 1/3 are major mediators. "
12/01/2011 - "The common mechanism by which inactivation of Casp8 induces liver necrosis in both injury models involves the formation of protein complexes that included the adaptor protein Fas-associated protein with death domain and the kinases receptor-interacting protein (RIP) 1 and RIP3-these have been shown to be required for programmed necrosis. "
01/31/2013 - "We examined the role of receptor interacting protein (RIP) 3, a mediator of necrotic cell death, in atherosclerosis and found that RIP3(-/-);Ldlr(-/-) mice were no different from RIP3(+/+);Ldlr(-/-) mice in early atherosclerosis but had significant reduction in advanced atherosclerotic lesions. "
01/01/2012 - "Based on the findings that nicotinamide treatment decreased protein expression of receptor-interacting protein (RIP; a marker for cell necrosis) and cleaved caspase-3 (CC3; a marker for cell apoptosis) in normoxic cardiomyocytes, we found that it dramatically reduced hypoxia-induced necrosis and apoptosis in cardiomyocytes. "
|4.||Acute Liver Failure (Fulminant Hepatic Failure)
03/21/2014 - "The present study investigated the role of receptor interacting protein (RIP)1, a critical mediator of necroptosis, on AIF-dependent necroptosis during APAP-induced acute liver failure. "
03/21/2014 - "Role of receptor interacting protein (RIP)1 on apoptosis-inducing factor-mediated necroptosis during acetaminophen-evoked acute liver failure in mice."
07/01/2008 - "In the present study, we used mitochondrial DNA-depleted Jurkat subclones (rho0 cells) to demonstrate that Fas agonistic Ab (CH-11), at the concentrations that evoke apoptotic death of the parental Jurkat cells, induced necrosis mainly through generation of excess reactive oxygen species, lysosomal rupture, and sequential activation of cathepsins B and D, and in minor part through activation of receptor-interacting protein (RIP). "
|1.||Caspase 3 (Caspase-3)
|4.||Reactive Oxygen Species (Oxygen Radicals)
|5.||Mitochondrial DNA (mtDNA)
|8.||Caspase 8 (Caspase-8)
|9.||Proteins (Proteins, Gene)
|10.||Type I Tumor Necrosis Factor Receptors