ArticleBiophysical journal2006
Biophysical properties of the apoptosis-inducing plasma membrane voltage-dependent anion channel.
Article in Biophysical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Microglial Histaminergic Signaling Promotes Interleukin-10 Production and Ameliorates Motor Dysfunction in Parkinson's Disease.Aging and disease · 2025Article
- The ATP-Releasing Maxi-Cl Channel: Its Identity, Molecular Partners and Physiological/Pathophysiological Implications.Life (Basel, Switzerland) · 2021Review
- Vascular endothelial growth factor signaling requires glycine to promote angiogenesis.Scientific reports · 2017Article
- The properties, functions, and pathophysiology of maxi-anion channels.Pflugers Archiv : European journal of physiology · 2016Review
- A voltage dependent non-inactivating Na+ channel activated during apoptosis in Xenopus oocytes.PloS one · 2014Article
- σ-1 receptor at the mitochondrial-associated endoplasmic reticulum membrane is responsible for mitochondrial metabolic regulation.The Journal of pharmacology and experimental therapeutics · 2012Article
- Autophagy and apoptosis are differentially induced in neurons and astrocytes treated with an in vitro mimic of the ischemic penumbra.PloS one · 2012Article
- The maxi-anion channel: a classical channel playing novel roles through an unidentified molecular entity.The journal of physiological sciences : JPS · 2009Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ion channels in the plasma membrane play critical roles in apoptosis. In a recent study we found that a voltage-dependent anion channel in the plasma membrane (VDACpl) of neuronal hippocampal cell line (HT22) cells was activated during apoptosis and that channel block prevented apoptosis. Whether or not VDACpl is identical to the mitochondrial VDACmt has been debated. Here, we biophysically characterize the apoptosis-inducing VDACpl and compare it with other reports of VDACpls and VDACmt. Excised membrane patches of apoptotic HT22 cells were studied with the patch-clamp technique. VDACpl has a large main-conductance state (400 pS) and occasionally subconductance states of approximately 28 pS and 220 pS. The small subconductance state is associated with long-lived inactivated states, and the large subconductance state is associated with excision of the membrane patch and subsequent activation of the channel. The open-probability curve is bell shaped with its peak around 0 mV and is blocked by 30 microM Gd3+. The gating can be described by a symmetrical seven-state model with one open state and six closed or inactivated states. These channel properties are similar to those of VDACmt and other VDACpls and are discussed in relation to apoptosis.
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Registered trials
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