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In CollectionCell death and survival
Biochem J (2022) 479 (3): 357–384.
Published: 11 February 2022
... are engaged by their ligands (the extrinsic pathway) or when BCL-2-family pro-apoptotic proteins cause the permeabilization of the mitochondrial outer membrane (the intrinsic pathway). Both the intrinsic and extrinsic pathways of apoptosis lead to the activation of a family of proteases, the caspases, which...
Biochem J (2021) 478 (17): 3179–3184.
Published: 07 September 2021
...Amy M. Weeks Apoptosis is a cell death program that is executed by the caspases, a family of cysteine proteases that typically cleave after aspartate residues during a proteolytic cascade that systematically dismantles the dying cell. Extensive signaling crosstalk occurs between caspase-mediated...
Biochem J (2003) 370 (3): 1027–1032.
Published: 15 March 2003
... of nitrobenzylthioinosine, a nucleoside-transport inhibitor, completely protects Jurkat cells from apoptosis. Adenosine, but not other nucleosides, also protects Jurkat cells from AICAriboside-induced apoptosis. The apoptotic effect is caspase-dependent since caspases 9 and 3 are activated and the caspase inhibitor...
Biochem J (2000) 347 (2): 543–551.
Published: 10 April 2000
... remaining attached were growth-arrested and developed features of senescence in 1 week. The detached cells showed caspase-3 activation and typical morphological changes associated with apoptosis. Caspase-3 activation was H 2 O 2 dose-dependent and preceded nuclear condensation or plasma membrane leakage...
Biochem J (1999) 338 (2): 295–303.
Published: 22 February 1999
... NO donors or when NO • was generated by inducible NO synthase activation, and was evident at the level of p53 accumulation, caspase activation and DNA fragmentation. Stimulation of parent and SOD-overexpressing cells with a combination of lipopolysaccharide and murine interferon γ produced equivalent...