ArticleThe Journal of cell biology2001
The channel of death.
Article in The Journal of cell biology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
6 citing papers in PubMed.
- Apoptosis as a mechanism for cell surface expression of the autoantigen pyruvate dehydrogenase complex.Clinical and experimental immunology · 2004Article
- Expression of expanded polyglutamine protein induces behavioral changes in Drosophila (polyglutamine-induced changes in Drosophila).Cellular and molecular neurobiology · 2004Article
- Modulation of synaptic transmission by the BCL-2 family protein BCL-xL.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Spatial and temporal changes in Bax subcellular localization during anoikis.The Journal of cell biology · 2003Article
- Molecular pathways in cerebral ischemia: cues to novel therapeutic strategies.Molecular neurobiology · 2003Review
- Mitochondrial respiratory control is lost during growth factor deprivation.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
Corrections and comments
- Comment on
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The proapoptotic members of the Bcl-2 family have been proposed to participate in the formation of a channel that releases these apoptogenic factors when mitochondria receive apoptotic signals. A recent study provides the first direct, biophysical measurement of a potentially apoptosis-specific mitochondrial channel, which is regulated by Bcl-2 family members and may play a primary role in the release of the proapoptotic factors.
Indexed as
Identifiers
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.