Apoptosis signaling.

By A. Strasser, L. O’Connor, V. Dixit. Annual Review of Biochemistry, 2000

1,146 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/03ed066b43d9ac79d835f1c0790213857d8b78f1

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology

1. Suzanne Cory
2. Jerry M. Adams
3. S. Nagata
4. P. Jost
5. A. Strasser
6. Marcel Leist
7. M. Jäättelä
8. T. Kanneganti

In Molecular Biology

1. Jerry M. Adams
2. Suzanne Cory
3. A. Strasser
4. S. Nagata
5. P. Jost
6. M. Jäättelä
7. Zheng Dong
8. Marcel Leist

In Nutrition and Dietetics

1. S. Nagata
2. P. Jost
3. A. Strasser

Citations in the corpus

• The Bcl-2 apoptotic switch in cancer development and therapy (2007, background): “Some of these issues are discussed more extensively in earlier reviews (Strasser et al., 2000; Cory and Adams, 2002; Adams, 2003; Cory et al., 2003; Danial and Korsmeyer, 2004; Fesik, 2005; Strasser, 2005).”
• Pathophysiology of Cisplatin-Induced Acute Kidney Injury (2014, background): “In the extrinsic pathway, activation of death receptors such as Fas and tumor necrosis factor-alpha (TNFR) leads to activation of downstream caspases to induce apoptosis [32].”
• Keeping killers on a tight leash: transcriptional and post-translational control of the pro-apoptotic activity of BH3-only proteins (2002, background): “elegans CED-9 prevents CED-3 caspase activation by blocking its adapter CED-4.(1) Since Bcl-2 and its pro-survival relatives do not bind to Apaf-1,(14,15) mammalian Bcl-2-like molecules would have to interact with other adapters that activate `initiator caspases' other than caspase-9.”
• Cisplatin nephrotoxicity: mechanisms and renoprotective strategies. (2008, background): “In the extrinsic pathway, binding of the death receptors by ligands at the plasma membrane leads to the recruitment and activation of caspase-8, which further activate downstream caspases to induce apoptosis.(45) Major death receptors include Fas, tumor-necrosis factor-a (TNF-a) receptor (TNFR) 1 an”
• Cytochrome c binds to inositol (1,4,5) trisphosphate receptors, amplifying calcium-dependent apoptosis (2003, background): “NATURE CELL BIOLOGY VOLUME 5 | NUMBER 12 | DECEMBER 2003 1051 Cytochrome c binds to inositol (1,4,5) trisphosphate receptors, amplifying calcium-dependent apoptosis Darren Boehning1,5, Randen L.”
• The many roles of FAS receptor signaling in the immune system (2009, positive): “…tumor cells, expression of dominant-negative FADD, CRMA, or c-FLIP had no impact on chemotherapeutic drug-induced killing of a collection of lymphoma-derived cell lines, demonstrating that FADD and caspase-8 are dispensable for this process in at least certain cancers (Strasser et al., 1995, 2000).”
• Four deaths and a funeral: from caspases to alternative mechanisms (2001, background): “Sensitization to TNF-induced apoptosis by 1,25dihydroxy vitamin D(3) involves up-regulation of the TNF receptor 1 and cathepsin B.”
• DAI complexes with RIP3 to mediate virus-induced programmed necrosis that is targeted by murine cytomegalovirus vIRA (2012, neutral): “Apoptosis is a well-recognized caspase-dependent host defense pathway triggered through cell-intrinsic as well as cell-extrinsic signals that also helps shape embryonic development (Hengartner, 2000; Strasser et al., 2000).”
• Get a ligand, get a life: integrins, signaling and cell survival (2002, neutral): “4) (Strasser et al., 2000).”
• Toll-like Receptor 3-mediated Necrosis via TRIF, RIP3, and MLKL* (2013, background): “Apoptosis depends on a caspase-dependent proteolytic cascade that dismantles cells in an orderly fashion while maintaining membrane integrity (12, 13), whereas programmed necrosis leads to cell leakage through mechanisms that are currently being defined.”