ArticleThe Biochemical journal2001
Elevated extracellular [K+] inhibits death-receptor- and chemical-mediated apoptosis prior to caspase activation and cytochrome c release.
Article in The Biochemical journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 101 citations in OpenAlex.
- Hydrogel-Based Delivery of Ion Channel Modulators for Cancer Therapy: Current Advances and Future Perspectives.Gels (Basel, Switzerland) · 2026Review
- Cancer as a Channelopathy-Appreciation of Complimentary Pathways Provides a Different Perspective for Developing Treatments.Cancers · 2022Review
- Synthetic NaChem · 2021Article
- Antiapoptotic Clone 11-Derived Peptides InduceJournal of virology · 2020Article
- Ions, the Movement of Water and the Apoptotic Volume Decrease.Frontiers in cell and developmental biology · 2020Review
- Regulation of interleukin-1 beta secretion from macrophages via modulation of potassium ion (KFEBS letters · 2019Article
- The Bioelectric Code: Reprogramming Cancer and Aging From the Interface of Mechanical and Chemical Microenvironments.Frontiers in cell and developmental biology · 2018Review
- Article
- The effect of K(+) on caspase activity of corneal epithelial cells exposed to UVB.Experimental eye research · 2016Review
- Bioelectrical regulation of cell cycle and the planarian model system.Biochimica et biophysica acta · 2015Review
- Mitochondrial and postmitochondrial survival signaling in cancer.Mitochondrion · 2014Review
- Ion channels and apoptosis in cancer.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
- A voltage dependent non-inactivating Na+ channel activated during apoptosis in Xenopus oocytes.PloS one · 2014Article
- Convergent Ca2+ and Zn2+ signaling regulates apoptotic Kv2.1 K+ currents.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Caspase-2 is an initiator caspase responsible for pore-forming toxin-mediated apoptosis.The EMBO journal · 2012Article
- Osmotic stress resistance imparts acquired anti-apoptotic mechanisms in lymphocytes.The Journal of biological chemistry · 2012Article
- Intracellular K+ concentration decrease is not obligatory for apoptosis.The Journal of biological chemistry · 2011Article
- Endothelial and smooth muscle cell ion channels in pulmonary vasoconstriction and vascular remodeling.Comprehensive Physiology · 2011Review
- Ion channel inhibitors block caspase activation by mechanisms other than restoring intracellular potassium concentration.Cell death & disease · 2011Article
- Life and death of lymphocytes: a volume regulation affair.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Efflux of intracellular K(+) and cell shrinkage are features of apoptosis in many experimental systems, and a regulatory role has been proposed for cytoplasmic [K(+)] in initiating apoptosis. We have investigated this in both death-receptor-mediated and chemical-induced apoptosis. Using Jurkat T cells pre-loaded with the K(+) ion surrogate (86)Rb(+), we have demonstrated an efflux of intracellular K(+) during apoptosis that was concomitant with, but did not precede, other apoptotic changes, including phosphatidylserine externalization, mitochondrial depolarization and cell shrinkage. To further clarify the role of K(+) ions in apoptosis, cytoprotection by elevated extracellular [K(+)] was studied. Induction of apoptosis by diverse death-receptor and chemical stimuli in two cell lines was inhibited prior to phosphatidylserine externalization, mitochondrial depolarization, cytochrome c release and caspase activation. Using a cell-free system, we have demonstrated a novel mechanism by which increasing [K(+)] inhibited caspase activation. In control dATP-activated lysates, Apaf-1 oligomerized to a biologically active caspase processing approximately 700 kDa complex and an inactive approximately 1.4 MDa complex. Increasing [K(+)] inhibited caspase activation by preventing formation of the approximately 700 kDa complex, but not of the inactive complex. Thus intracellular and extracellular [K(+)] markedly affect caspase activation and the initiation of apoptosis induced by both death-receptor ligation and chemical stress.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.