The DOI matches its Crossref record; 55 of the 55 references it cites were found in a registry or an index.
Cell Death Signaling
Open accessAbstract
In multicellular organisms, cell death is a critical and active process that maintains tissue homeostasis and eliminates potentially harmful cells. There are three major types of morphologically distinct cell death: apoptosis (type I cell death), autophagic cell death (type II), and necrosis (type III). All three can be executed through distinct, and sometimes overlapping, signaling pathways that are engaged in response to specific stimuli. Apoptosis is triggered when cell-surface death receptors such as Fas are bound by their ligands (the extrinsic pathway) or when Bcl2-family proapoptotic proteins cause the permeabilization of the mitochondrial outer membrane (the intrinsic pathway). Both pathways converge on the activation of the caspase protease family, which is ultimately responsible for the dismantling of the cell. Autophagy defines a catabolic process in which parts of the cytosol and specific organelles are engulfed by a double-membrane structure, known as the autophagosome, and eventually degraded. Autophagy is mostly a survival mechanism; nevertheless, there are a few examples of autophagic cell death in which components of the autophagic signaling pathway actively promote cell death. Necrotic cell death is characterized by the rapid loss of plasma membrane integrity. This form of cell death can result from active signaling pathways, the best characterized of which is dependent on the activity of the protein kinase RIP3.
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1 retracted
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“Recent studies have shown that components of the autophagy pathway can be recruited to phagosomes that have engulfed organisms or cells, facilitating the degradation of the phagocytosed cargo (Sanjuan et al. 2007; Martinez et al. 2011).”
BackgroundSelf-citationRetractedAMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1
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Autophagy and the Integrated Stress Response
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Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury
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AIM2 recognizes cytosolic dsDNA and forms a caspase-1-activating inflammasome with ASC
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Mitochondria and cell death: outer membrane permeabilization and beyond
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Self-citationNon-canonical inflammasome activation targets caspase-11
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Cited by
Galluzzi, L., Vitale, I., Aaronson, S. A., Abrams, J. M., Adam, D., Agostinis, P., Alnemri, E. S., Altucci, L., Amelio, I., Andrews, D. W., et al. (2018) · Cell Death & Differentiation · doi:10.1038/s41418-017-0012-4 · Cited by 6,680
Self-citationActivation of apoptosis signalling pathways by reactive oxygen species
Redza-Dutordoir, M., & Averill-Bates, D. A. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2016.09.012 · Cited by 3,731
Reactive Oxygen Species-Induced Lipid Peroxidation in Apoptosis, Autophagy, and Ferroptosis
Su, L.-J., Zhang, J.-H., Gomez, H., Murugan, R., Hong, X., Xu, D., Jiang, F., & Peng, Z.-Y. (2019) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2019/5080843 · Cited by 2,166
Apoptosis: A Target for Anticancer Therapy
Pfeffer, C., & Singh, A. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19020448 · Cited by 1,542
Signaling in innate immunity and inflammation
Newton, K., & Dixit, V. M. (2012) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a006049 · Cited by 1,513
Metadata
- Authors
- Green, D. R., & Llambi, F.
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2015-12
- Volume
- 7
- Issue
- 12
- Pages
- a006080
- ISSN
- 1943-0264 (ISSN-L)
- OpenAlex
- W2272315791
- Cited by
- 1,101
- References
- 55
- Type
- posted content
- Language
- en
- Open access
- bronze
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