Necroptosis: the release of damage-associated molecular patterns and its physiological relevance.
By A. Kaczmarek, Peter Vandenabeele, D. Krysko. Immunity, 2013
1,362 citations recorded by the source corpus.
Subfields: Molecular Biology, Nutrition and Dietetics
View Paper: https://www.semanticscholar.org/paper/4ad2ca0255e081ed91d244cfcf221cae499354b3
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In Molecular Biology
- Brent R. Stockwell
- Scott J. Dixon
- W. Yang
- Qing-zhang Tuo
- P. Lei
- Beth Levine
- Shu-ting Zhang
- Douglas R. Green
In Nutrition and Dietetics
- Brent R. Stockwell
- Scott J. Dixon
- W. Yang
- Beth Levine
- Douglas R. Green
- D. Tang
- R. Kang
- James A. Olzmann
Citations in the corpus
- Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications (2021, background): “The TNF family of cytokines can recruit activate caspase‐8 through the adaptor protein FADD, further triggering apoptosis; however, under certain conditions, suppression of caspase‐8 or FADD increases the sensitivity to these cytokines, causing necroptosis.(86,87) Necroptosis is regulated necrotic c”
- Global Survey of Cell Death Mechanisms Reveals Metabolic Regulation of Ferroptosis (2016, methodology): “FIN56 Target Identification Conjugation of active and inactive probes with Profinity Epoxide Resin—6 μmol of Active (SRS11-31) or inactive (SRS11-66) probes dissolved in 500 μL DMSO and 300mg of Profinity™ Epoxide Resin (Bio-Rad) were incubated in saturated sodium bicarbonate at 45 °C for 3 days.”
- The Development of the Concept of Ferroptosis (2018, neutral): “normal physiological functions, such as the modulation of inflammation and the maintenance of adult T-cell homeostasis [15,21,22], and may”
- Inflammation and aging: signaling pathways and intervention therapies (2023, background): “However, necroptosis triggers inflammation through the massive release of DAMPs from the disintegrating cell.(237) Fig.”
- To be or not to be? How selective autophagy and cell death govern cell fate. (2014, positive): “Under conditions in which TNFR1 is engaged but caspase-8-FLIP activity is blocked or disrupted, the RIPK3-MLKL interaction is promoted to cause necrotic cell death (Kaczmarek et al., 2013) through an effector mechanism that remains elusive but is likely to involve the plasma membrane.”
- Necroptosis: a regulated inflammatory mode of cell death (2018, background): “Numerous in vitro studies have reported that inhibition of caspase-8 molecules resulted in activation of RIPK3, a key player of necroptosis [6, 7, 23].”