Results 201 to 210 of about 162,682 (253)
Cell Death and Differentiation, 1999 Caspases are the key effector molecules of the physiological death process known as apoptosis, although some are involved in activation of cytokines, rather than cell death. They exist in most of our cells as inactive precursors (zymogens) that kill the cell once activated. Caspases can be controlled in two ways.
Paul G Ekert, John Silke, David L Vaux
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Screening for Caspase-3 Inhibitors: A New Class of Potent Small-Molecule Inhibitors of Caspase-3 [PDF]
Journal of Biomolecular Screening, 2006 From the authors' 650,000 compound collection, they have selected approximately 15,000 potential small-molecule protease inhibitors, which were subjected to high-throughput screening against caspase-3. The screening yielded a series of hits that belong to 11 different scaffolds.
Ilya Okun +2 more
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Caspase inhibitors: viral, cellular and chemical [PDF]
Cell Death and Differentiation, 2006 Caspases, key mediators of apoptosis, are a structurally related family of cysteine proteases that cleave their substrates at aspartic acid residues either to cause cell death or to activate cytokines as part of an immune response. They can be controlled upstream by the regulation of signals that lead to zymogen activation, or downstream by inhibitors ...
David L Vaux, Vaux D L
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Caspases and caspase inhibitors
Trends in Biochemical Sciences, 1997Five years ago, little was known about mechanisms of apoptotic execution. Now, one class of cell-death gene, the cysteine and aspartases (caspases) has come under intensive study. This review discusses the two classes of caspases, the reasons why humans may have so many caspase genes, the growing list of caspase substrates, and viral and ...
P, Villa, S H, Kaufmann, W C, Earnshaw
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Neuroprotection by caspase inhibitors
Expert Opinion on Investigational Drugs, 1999In the majority of brain diseases, apoptosis causes or exacerbates neuronal damage. Caspases are the final executioners of the apoptotic cell death programme. This family of proteases is implicated in the pathogenesis of many forms of brain damage, including those induced by ischaemia, inflammation or trauma, as well as those arising in Alzheimer's ...
, Braun, , Tuomanen, , Cleveland
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Caspase inhibitors as neuroprotective agents
Expert Opinion on Emerging Drugs, 2001Apoptotic neuronal cell death has been demonstrated to occur in the central nervous system (CNS), following both acute injury and during chronic neurodegenerative conditions. Currently, the majority of experimental evidence for a role of caspases in CNS damage has been established following acute neuronal insults, including ischaemic stroke, traumatic ...
Joseph A Erhardt
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Prospects for Caspase Inhibitors
Mini-Reviews in Medicinal Chemistry, 2004Programmed cell death, or apoptosis, is executed by a series of Cysteine Aspartyl Proteases (Caspases) that form a proteolytic cascade. Each caspase functions either to activate downstream caspases by proteolytic cleavage and/or to proteolytically cleave cellular substrates.
Tom, O'Brien, Dennis, Lee
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Endogenous Inhibitors of Caspases
Journal of Clinical Immunology, 1999Caspases are cysteine proteases that are specific for aspastic acid residues. These enzymes have been extensively characterized as integral and highly conserved components of a variety of cell death programs. Cowpox and several insect viruses have evolved mechanisms that counter host cell suicide by encoding proteins that directly inhibit caspases ...
Q L, Deveraux +3 more
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Controlled Inhibition of Apoptosis by Photoactivatable Caspase Inhibitors [PDF]
Cell Chemical Biology, 2020 Caspases control regulated cell death (apoptosis), a process that is crucial in the development of multicellular organisms as well as in various diseases. In order to spatiotemporally study apoptosis, we here develop photoactivatable caspase inhibitors.
Steven H L Verhelst
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The Neuroscientist, 2012
In ischemic stroke, apoptosis persists for days to weeks after the onset of an ischemic event. Cysteine-ASPartic proteASEs (caspases) are key mediators of apoptosis and neurodegeneration in stroke. The impact of caspase activity is not restricted to neuronal death, as caspases can exacerbate inflammation and alter glial function.
Nsikan, Akpan, Carol M, Troy
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In ischemic stroke, apoptosis persists for days to weeks after the onset of an ischemic event. Cysteine-ASPartic proteASEs (caspases) are key mediators of apoptosis and neurodegeneration in stroke. The impact of caspase activity is not restricted to neuronal death, as caspases can exacerbate inflammation and alter glial function.
Nsikan, Akpan, Carol M, Troy
openaire +2 more sources