Cell Death Signaling.
By Douglas R. Green, F. Llambi. Cold Spring Harbor Perspectives in Biology, 2015
1,019 citations recorded by the source corpus.
Subfields: Cell Biology, Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/91544256876ff4ec820589647d7e61e48dd9588e
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Citations in the corpus
- Understanding MAPK Signaling Pathways in Apoptosis (2020, background): “Generally, caspases can be activated by either an extrinsic pathway or an intrinsic pathway; the former is initiated by cell-surface death receptors stimulated by their corresponding ligands, and the latter is induced by protein release from the mitochondrial outer membrane due to pro-apoptotic Bcl-”
- Signal transduction in cancer. (2015, neutral): “…rearrangements in B lymphocytes, and this contributes to follicular lymphoma by preventing cells from undergoing apoptosis. p53 also regulates apoptosis, both by inducing transcription of proapoptotic regulators and binding directly to the proapoptotic protein Bax (Green and Llambi 2014).”
- Reactive Oxygen Species-Induced Lipid Peroxidation in Apoptosis, Autophagy, and Ferroptosis (2019, background): “Apoptosis is triggered when the Bcl2-family proapoptotic proteins cause the opening of mitochondrial permeability transition pore and proapoptotic proteins into cytoplasm by interacting with apoptotic protease-activating factor 1 (Apaf-1) and procaspase-9 to constitute apoptosome [56, 57].”
- Apoptosis: A Target for Anticancer Therapy (2018, background): “In the extrinsic pathway, the activation of caspase-8 leads to the activation of BH3 interacting-domain death agonist (BID), a BH3-only protein [12].”