Caspase Inhibitors
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Subject Areas on Research
- A GH3-like domain in reaper is required for mitochondrial localization and induction of IAP degradation.
- A non-transformed oligodendrocyte precursor cell line, OL-1, facilitates studies of insulin-like growth factor-I signaling during oligodendrocyte development.
- A novel ubiquitin fusion system bypasses the mitochondria and generates biologically active Smac/DIABLO.
- A20 protects endothelial cells from TNF-, Fas-, and NK-mediated cell death by inhibiting caspase 8 activation.
- Alpha-fodrin is cleaved by caspase-3 in a chronic ocular hypertensive (COH) rat model of glaucoma.
- Analysis of candidate antagonists of IAP-mediated caspase inhibition using yeast reconstituted with the mammalian Apaf-1-activated apoptosis mechanism.
- Angiotensin II attenuates chemical hypoxia-induced caspase-3 activation in primary cortical neuronal cultures.
- Antifibrotic therapies: will we ever get there?
- Baculoviral IAP repeat-containing-4 protects optic nerve axons in a rat glaucoma model.
- Bortezomib inhibits PKR-like endoplasmic reticulum (ER) kinase and induces apoptosis via ER stress in human pancreatic cancer cells.
- Bortezomib sensitizes pancreatic cancer cells to endoplasmic reticulum stress-mediated apoptosis.
- Calpain mediates ischemic injury of the liver through modulation of apoptosis and necrosis.
- Caspase 3 in dying tumor cells mediates post-irradiation angiogenesis.
- Caspase-8 and caspase-3 small interfering RNA decreases ischemia/reperfusion injury to the liver in mice.
- Cyclosporin A inhibits chromium(VI)-induced apoptosis and mitochondrial cytochrome c release and restores clonogenic survival in CHO cells.
- Differential apoptosis-inducing effect of quercetin and its glycosides in human promyeloleukemic HL-60 cells by alternative activation of the caspase 3 cascade.
- Dying glioma cells establish a proangiogenic microenvironment through a caspase 3 dependent mechanism.
- Emodin induces apoptosis in human promyeloleukemic HL-60 cells accompanied by activation of caspase 3 cascade but independent of reactive oxygen species production.
- Endothelial cell surface ATP synthase-triggered caspase-apoptotic pathway is essential for k1-5-induced antiangiogenesis.
- Evidence that non-caspase proteases are required for chromatin degradation during apoptosis.
- Extracellular caspase-6 drives murine inflammatory pain via microglial TNF-α secretion.
- Fatty liver vulnerability to endotoxin-induced damage despite NF-kappaB induction and inhibited caspase 3 activation.
- Generation of neuronal intranuclear inclusions by polyglutamine-GFP: analysis of inclusion clearance and toxicity as a function of polyglutamine length.
- High and low molecular weight DNA cleavage in ovarian granulosa cells: characterization and protease modulation in intact cells and in cell-free nuclear autodigestion assays.
- High-fat/high-cholesterol diet promotes a S1P receptor-mediated antiapoptotic activity for VLDL.
- IAP proteins: sticking it to Smac.
- Induction of apoptosis by the novel retinoid AHPN in human T-cell lymphoma cells involves caspase-dependent and independent pathways.
- Inhibition of fetal thymic caspases abrogates the consequences of adenosine deaminase deficiency.
- Interferon regulatory factors regulate interleukin-1beta-converting enzyme expression and apoptosis in vascular smooth muscle cells.
- Mechanisms of ischemic injury are different in the steatotic and normal rat liver.
- Molecular cloning of ILP-2, a novel member of the inhibitor of apoptosis protein family.
- Neonatal infection-induced memory impairment after lipopolysaccharide in adulthood is prevented via caspase-1 inhibition.
- Pan-caspase inhibitor VX-166 reduces fibrosis in an animal model of nonalcoholic steatohepatitis.
- Removal of the pro-domain does not affect the conformation of the procaspase-3 dimer.
- Repetitive intraperitoneal caspase-3 inhibitor and anesthesia reduces neuronal damage.
- Scientific and clinical challenges in sepsis.
- Smac/Diablo antagonizes ubiquitin ligase activity of inhibitor of apoptosis proteins.
- The IAP proteins: caspase inhibitors and beyond.
- The combination of TPL2 knockdown and TNFα causes synthetic lethality via caspase-8 activation in human carcinoma cell lines.
- The deubiquitinating enzyme DUBAI stabilizes DIAP1 to suppress Drosophila apoptosis.
- The injured cochlea as a target for inflammatory processes, initiation of cell death pathways and application of related otoprotectives strategies.
- The p35 relative, p49, inhibits mammalian and Drosophila caspases including DRONC and protects against apoptosis.
- The release of microparticles and mitochondria from RAW 264.7 murine macrophage cells undergoing necroptotic cell death in vitro.
- The release of microparticles by RAW 264.7 macrophage cells stimulated with TLR ligands.
- The small heat shock protein alpha B-crystallin is a novel inhibitor of TRAIL-induced apoptosis that suppresses the activation of caspase-3.
- Uncoupling of the signaling and caspase-inhibitory properties of X-linked inhibitor of apoptosis.
- Upstream regulatory role for XIAP in receptor-mediated apoptosis.
- XIAP as target for therapeutic apoptosis in prostate cancer.
- Xaf1 can cooperate with TNFalpha in the induction of apoptosis, independently of interaction with XIAP.
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Keywords of People
- Choi, Steven Sok, Associate Professor of Medicine, Medicine, Gastroenterology