Elevated extracellular [K+] inhibits death-receptor- and chemical-mediated apoptosis prior to caspase activation and cytochrome c release

Biochemical Journal

Volumn 357, Issue 1, 2001, Pages 137-145

  Thompson, G J ^a   Langlais, C ^a   Cain, K ^a   Conley, E C ^a   Cohen, G M ^a  

^a UNIVERSITY OF LEICESTER   (United Kingdom)

Author keywords

Apaf 1; Apoptosome; CD95; Cytoprotection; Jurkat cells

Indexed keywords

ADENOSINETRIPHOSPHATE; CELL CULTURE; CYTOLOGY; OLIGOMERS;

CHEMICAL STRESSES;

BIOCHEMISTRY;

ADENOSINE TRIPHOSPHATE; APOPTOSIS INDUCING FACTOR; APOPTOSIS INHIBITOR; APOPTOTIC PROTEASE ACTIVATING FACTOR 1; CASPASE; CYTOCHROME C; PHOSPHATIDYLSERINE; POTASSIUM ION; PROTEINASE ACTIVATED RECEPTOR 1; RUBIDIUM 86; UNCLASSIFIED DRUG;

APOPTOSIS; ARTICLE; CELL DEATH; CELL FREE SYSTEM; CELL PROTECTION; CELL STIMULATION; CELL STRUCTURE; CONTROLLED STUDY; CYTOPLASM; ENZYME ACTIVATION; ENZYME REGULATION; ENZYME RELEASE; HUMAN; HUMAN CELL; HYSTERESIS; INTRACELLULAR TRANSPORT; MEMBRANE DEPOLARIZATION; OLIGOMERIZATION; POTASSIUM CELL LEVEL; POTASSIUM TRANSPORT; PRIORITY JOURNAL; PROTEIN PROCESSING;

AMINO ACID CHLOROMETHYL KETONES; ANTIBODIES; ANTIGENS, CD95; APOPTOSIS; CASPASES; CYSTEINE PROTEINASE INHIBITORS; CYTOCHROME C GROUP; CYTOSOL; ENZYME ACTIVATION; ETOPOSIDE; EXTRACELLULAR SPACE; FLOW CYTOMETRY; HUMANS; INTRACELLULAR MEMBRANES; JURKAT CELLS; KINETICS; MEMBRANE POTENTIALS; MITOCHONDRIA; PHOSPHATIDYLSERINES; POTASSIUM; POTASSIUM CHLORIDE; RECEPTORS, TUMOR NECROSIS FACTOR; RUBIDIUM; T-LYMPHOCYTES; TUMOR CELLS, CULTURED;

EID: 0035397708     PISSN: 02646021     EISSN: None     Source Type: Journal    
DOI: 10.1042/0264-6021:3570137     Document Type: Article

References (42)

1. Cell death: The significance of apoptosis
2. + efflux in the activation of apoptosis
3. Changes in elemental content during apoptotic cell death studied by electron probe X-ay microanalysis
4. + and cell shrinkage
5. Plasma membrane potential in thymocyte apoptosis
6. Normotonic cell shrinkage because of disordered volume regulation is an early prerequisite to apoptosis
7. + suppresses the activation of apoptosis in lymphocytes
8. Potassium leakage during the apoptotic degradation phase
9. Caspases: The executioners of apoptosis
10. Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonucleases activation
11. Apoptosis in cerebellar granule cells is blocked by high KCl, forskolin, and IGF-1 through distinct mechanisms of action: The involvement of intracellular calcium and RNA synthesis
12. + ratio blocks apoptosis in vascular smooth muscle at a site upstream of caspase 3
13. Membrane depolarisation and depletion of intracellular calcium stores are associated with delay of apoptosis in human neutrophils
14. Cytotoxicity-dependent APO-1 (Fas/CD95)-associated proteins form a death-inducing signalling complex (DISC) with the receptor
15. FLICE is activated by association with the CD95 death-inducing signalling complex
16. Two CD95 (APO-1/Fas) signalling pathways
17. Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis
18. Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis
19. The release of cytochrome c from mitochondria: A primary site for Bcl-2 regulation of apoptosis
20. Mitochondria and apoptosis
21. Cytoohrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade
22. Cytochrome c and dATP-mediated oligomerization of Apaf-1 is a prerequisite for procaspase-9 activation
23. An APAF-1 cytochrome c multimeric complex is a functional apoptosome that activates procaspase-9
24. Caspase activation involves the formation of the aposome, a large (≈ 700 kDa) caspase activating complex
25. Apaf-1 oligomerises into biologically active ∼ 700-kDa and inactive 1.4-MDa apoptosome complexes
26. Distinct caspase cascades are initiated in receptor-mediated and chemical-induced apoptosis
27. Identification and molecular cloning of two novel receptors for the cytotoxic ligand TRAIL
28. Protease involvement in fodrin cleavage and phosphatidylserine exposure in apoptosis
29. Measurement of mitochondrial membrane potential using fluorescent rhodamine derivatives
30. Processing/activation of at least four interleukin-1β converting-enzyme-like proteases occurs during the execution phase of apoptosis in human monocytic tumour cells
31. Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarisation
32. An interleukin-1β-converting enzyme-like protease is a common mediator of apoptosis in thymocytes
33. FLICE is predominantly expressed as two functionally active isoforms, caspase-8/a and caspase-8/b
34. CPP32, a novel human apoptotic protein with homology to Caenorhabditis elegans cell death protein Ced-3 and mammalian interleukin-1β-converting enzyme
35. Mitochondrai and programmed cell death: Back to the future
36. JNK (c-Jun N-terminal kinase) and p38 activation in receptor-mediated and chemically induced apoptosis of T-cells: Differential requirements for caspase activation
37. Absence of volume regulatory mechanisms contributes to the rapid activation of apoptosis in thymocytes
38. Activation of potassium and chloride channels by tumor necrosis factor α
39. Cell death induced by topoisomerase-targeted drugs: More questions than answers
40. Distinct pathways for stimulation of cytochrome c release by etoposide
41. + in HeLa cells
42. Sequence of metabolic changes during X-ray-induced apoptosis