Necrosis: a specific form of programmed cell death?
By S. Proskuryakov, A. G. Konoplyannikov, V. Gabai. Experimental Cell Research, 2003
734 citations recorded by the source corpus.
Subfields: Epidemiology, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/5c1b33ec743aa62e62bd7e7bc69ca7a1ecc49820
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Epidemiology
- E. White
- Robin Mathew
- Susan A. Elmore
- Guanghua Chen
- Shengkan Jin
- T. Vanden Berghe
- Peter Vandenabeele
- Alec C. Kimmelman
In Immunology
In Molecular Biology
- E. White
- Peter Vandenabeele
- Robin Mathew
- T. Vanden Berghe
- Susan A. Elmore
- Shengkan Jin
- Guido Kroemer
- Alec C. Kimmelman
Citations in the corpus
- Autophagy promotes tumor cell survival and restricts necrosis, inflammation, and tumorigenesis. (2006, background): “A third means to achieve cell death is by necrosis, which usually is associated with physical insults, failure of osmotic regulation, ATP depletion, HMGB1 release, cell lysis, and an inflammatory response that may facilitate wound healing (Kanduc et al., 2002; Majno and Joris, 1995; Nelson and White”
- Apoptosis: A Review of Programmed Cell Death (2007, background): “There are necrotic-like phenotypes that require gene activation and protein synthesis so they are, strictly speaking, forms of programmed cell death (Proskuryakov et al., 2003).”
- Necrosis, a well-orchestrated form of cell demise: signalling cascades, important mediators and concomitant immune response. (2006, background): “The late uptake of necrotic cells allows the dying cells to activate pro-inflammatory and immuno-stimulatory responses [18] whereas apoptotic cell death is immunologically and inflammatorily silent [188].”