The DOI matches its Crossref record; 80 of the 80 references it cites were found in a registry or an index.
Toward an understanding of the molecular mechanisms of physiological cell death.
Open accessAbstract
Cell death is a normal physiological process. Morphological studies have shown that cells that die by physiological mechanisms often undergo characteristic changes termed "apoptosis" or "programmed cell death." Recent work has begun to unravel the molecular mechanisms of these deaths and has shown that one of the primary cell-death pathways is conserved throughout much of evolution. In the nematode Caenorhabditis elegans programmed cell deaths are mediated by a mechanism controlled by the ced-9 gene; in mammals apoptosis can often be inhibited by expression of the bcl-2 gene. The ability of the human BCL2 gene to prevent cell deaths in C. elegans strongly suggests that bcl-2 and ced-9 are homologous genes. Although the process of cell death controlled by bcl-2 can occur in many cell types, there appears to be more than one physiological cell-death mechanism. Targets of cytotoxic T cells and cells deprived of growth factor both exhibit changes characteristic of apoptosis, such as DNA degradation. However, bcl-2 expression protects cells from factor withdrawal but fails to prevent cytotoxic T-cell killing. DNA degradation is, thus, not specific for any one cell-death mechanism. The ability of bcl-2 to protect cells from a wide variety of pathological, as well as physiological, stimuli indicates that many triggers can serve to activate the same suicide pathway, even some thought to cause necrosis, and not physiological cell death.
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Cites
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Cited by
Massive Cell Death of Immature Hematopoietic Cells and Neurons in Bcl-x-Deficient Mice
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Axon degeneration mechanisms: Commonality amid diversity
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Embryonic origin of hemocytes and their relationship to cell death in Drosophila
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Metadata
- Authors
- Vaux, D. L.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 1993-02
- Volume
- 90
- Issue
- 3
- Pages
- 786-789
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2015005447
- Cited by
- 608
- References
- 80
- FWCI
- 30.85
- Type
- journal article
- Language
- en
- Open access
- green
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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