Non-methylated competitive and irreversible inhibitor of caspase-1, as well as other caspases, which can be used directly with purified enzymes. It does not require esterase to hydrolyze the O-methyl ester like the cell-permeable form, Z-Val-Ala-Asp(OMe) fluoromethyl ketone (Product Code V-116).
Leistungsmerkmale und Vorteile
This compound is featured on the Caspases page of the Handbook of Receptor Classification and Signal Transduction. To browse other handbook pages, click here.
Signal transduction and targeted therapy, 5(1), 56-56 (2020-05-21)
Latent membrane protein 1 (LMP1) is a major Epstein-Barr virus (EBV)-encoded oncoprotein involved in latency infection that regulates mitochondrial functions to facilitate cell survival. Recently, mitochondrial fission has been demonstrated as a crucial mechanism in oncovirus-mediated carcinogenesis. Mitochondrial dynamin-related protein
JACC. Basic to translational science, 4(3), 304-317 (2019-07-18)
CANTOS (Canakinumab Antiinflammatory Thrombosis Outcome Study) confirmed interleukin (IL)-1β as an appealing therapeutic target for human atherosclerosis and related complications. However, there are serious gaps in our understanding of IL-1 production in atherosclerosis. Herein the authors show that complex plaques
Mature neutrophils must be quickly removed from inflammatory sites to prevent tissue damage. Neutrophil removal is thought to be accomplished primarily through caspase-dependent apoptosis, which involves several genes of mitochondrial origin. However, mature neutrophils show reduced gene transcription and mitochondrial
Frontiers in pharmacology, 13, 854526-854526 (2022-06-07)
Aloe-emodin (1,8-dihydroxy-3-hydroxymethyl-anthraquinone), derived from some Chinese edible medicinal herbs, exerts a potential anticancer activity on various cancer cells, making it a drug candidate for cancer therapy. Yet, the role of aloe-emodin in pyroptosis, a new type of cell death, is
EBV infection is a recognized epigenetic driver of carcinogenesis. We previously showed that EBV could protect cancer cells from TNF-induced necroptosis. This study aims to explore the epigenetic mechanisms allowing cancer cells with EBV infection to escape from RIP3-dependent necroptosis.
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