Results 251 to 260 of about 231,701 (306)
Targeting TLR4 Attenuates Endometriosis Progression by Suppressing NF-κB/NLRP3 Inflammasome Activation and Angiogenesis. [PDF]
Int J Mol SciCao Y, Zhu X, Hou X, Ding D.
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Effects of Arylsulfatase B and Pembrolizumab in combination on progression of metastatic melanoma in the B16F10 syngeneic mouse model. [PDF]
Front OncolBhattacharyya S +2 more
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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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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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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
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Caspase inhibitors as neuroprotective agents
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 ...
J J, Legos, D, Lee, J A, Erhardt
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Serine protease inhibitor 2A inhibits caspase-independent cell death [PDF]
FEBS Letters, 2004 The release of cysteine cathepsins from the lysosome into the cytoplasm can trigger programs of cell death (PCD) that do not require caspase executioner proteases but instead are mediated by toxic reactive oxygen species (ROS).
Wang, Yue +5 more
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