A novel pathway combining calreticulin exposure and ATP secretion in immunogenic cancer cell death
By Abhishek D Garg, D. Krysko, T. Verfaillie, A. Kaczmarek, G. B. Ferreira, T. Marysael, N. Rubio, M. Firczuk, C. Mathieu, A. Roebroek and 5 more. EMBO Journal, 2012
734 citations recorded by the source corpus.
Subfields: Biomedical Engineering, Cell Biology, Immunology
View Paper: https://www.semanticscholar.org/paper/116042165380ed946b871bcad3015596533a5c1c
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Biomedical Engineering
In Cell Biology
- Guido Kroemer
- Beth Levine
- D. Klionsky
- L. Galluzzi
- Douglas R. Green
- J. Cubillos-Ruiz
- Junying Yuan
- Y. Tsujimoto
In Immunology
Citations in the corpus
- Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “In line with a key role of CALR in the immunogenicity of RCD, the RNAi-mediated knockdown of CALR as well as natural defects in the CALR exposure pathway reportedly abolish the ability of dying cancer cells succumbing to anthracyclines to establish protective immunity in mice, whereas the exogenous ”
- Consensus guidelines for the detection of immunogenic cell death (2014, background): “Upon binding to low density lipoprotein receptorrelated protein 1 (LRP1, also known as CD91), membraneexposed CALR delivers a major phagocytic signal to professional antigen-presenting cells (APCs) such as dendritic cells, de facto improving their capacity to take up dead cells and their corpses.(66”
- Mechanism of action of conventional and targeted anticancer therapies: reinstating immunosurveillance. (2013, background): “Other stimuli (e.g., hypericin-based photodynamic therapy) can cause CRT exposure through a distinct, more rapid pathway that relies on PERK but not on caspase-8 (Garg et al., 2012).”