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Inhibition of caspase-9 aggravates acute liver injury through suppression of cytoprotective autophagy.
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inducible caspase-9 (iC9) safety switch can eliminate CD19.CAR-Ts in a dose-dependent manner, allowing either a selective containment of CD19.CAR-T expansion in case of CRS or complete deletion on demand granting normal B cell reconstitution.
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Cepharanthine treatment reduced mitochondrial membrane potential and upregulated the level of cleaved caspases, including caspase-9 and caspase-3/7, in a dose-dependent fashion.
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Bcl-2-caspase-9 apoptosis pathway was clearly activated in the testis of asthmatic mice with the increased expression of apoptosis-related proteins.
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Inhibition of Caspase-9 restricted, while Apaf-1 promoted, Chlamydia pneumoniae infection in HEp-2, HeLa, and mouse epithelial fibroblast (MEF) cells.
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The study demonstrates sublethal caspase-activation has an important role in cardiomyocyte differentiation and may have significant implications for promoting cardiac regeneration after myocardial injury involving exogenous or endogenous cell sources.
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Casp6 knockout in YAC128 mice does not abolish the presence of the mutant HTT protein-586 fragment but ameliorates depression, body weight gain, IGF-1 and BDNF levels in YAC128 mice.
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study demonstrates that MMP-3 leads to caspase-9 activation and suggests that this occurs indirectly via a cytosolic protein, possibly involving Apaf-1
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caspase-9 mediates Puma activation to determine the threshold for overcoming chemoresistance in cancer cells.
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Casp9, the initiator caspase of the intrinsic apoptotic cascade, has a role in murine fetal and adult hematopoiesis
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Effect of cortisol on caspases in the co-cultured C2C12 and 3 T3-L1 cells.
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findings demonstrate that focal activation of caspase-9 and -3 at neuromuscular junctions is essentially responsible for subsynaptic DNA damage and apoptotic synaptic degeneration in slow-channel myasthenic syndrome
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The activity of caspase-3, -8 and -9 was significantly increased in the isoflurane-treated cells compared with the untreated cells.
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After activation by caspase-9, caspase-3 inhibits ROS production and is required for efficient execution of apoptosis, while effector caspase-7 is required for apoptotic cell detachment.
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The mitochondrial apoptotic pathway mediated by caspase 9 is constitutively activated in oocytes.
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DP T cell apoptosis following experimental T. cruzi acute infection is dependent on glucocorticoid stimulation, promoting caspase-8 and -9 activation
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caspase-9 activity is up-regulated by zVAD-fmk and is involved in an amplification loop of etoposide-induced cell death at the mitochondrial level in mouse embryonic fibroblasts.
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Both megakaryocytes and platelets possess a functional apoptotic caspase cascade downstream of Bcl-2 family-mediated mitochondrial damage. Caspase-9 is the initiator caspase, and its loss blocks effector caspase activation.
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Immunohistochemical expression of Bcl-2, p53 and caspase-9 in hypothalamus magnocellular centers of nNOS knockout mice following water deprivation
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Results identify a cancer-specific mechanism of hnRNP L phosphorylation and subsequent lowering of the caspase-9a/9b ratio, which is required for the tumorigenic capacity of non-small cell lung cancer cells.
