The Bcl-2 apoptotic switch in cancer development and therapy
By Jerry M. Adams, Suzanne Cory. Oncogene, 2007
2,202 citations recorded by the source corpus.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/cc87f7683849106342e910c53fd2f05c1676652c
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Citations in the corpus
- Mitochondrial dynamics and apoptosis. (2008, background): “Bcl-2 family proteins regulate the release of cytochrome c and other proteins through the outer mitochondrial membrane (OMM) (Adams and Cory 2007; Chipuk and Green 2008).”
- Selectivity by Small-Molecule Inhibitors of Protein Interactions Can Be Driven by Protein Surface Fluctuations (2015, neutral): “The critical step of disregulating apoptosis in tumor maintenance and chemoresistance has made certain members of this family exceptionally attractive targets for therapeutic intervention for many years, and in a variety of cancers [17].”
- Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies (2016, background): “Therefore, by mediating permeabilization of the mitochondrial membrane, the Bcl-2 proteins serve as an “apoptotic switch” [30].”
- Apoptosis and Molecular Targeting Therapy in Cancer (2014, background): “It is now clear that, through its dual role, cyclin E provides a physiological balance between cell proliferation and death of hematopoietic cells [161].”
- Tumor resistance to apoptosis (2009, background): “cates to mitochondria upon cleavage and causes cytochrome c release.(7) The mitochondrial pathway is initiated by the release of”
- Role of Bcl-2 family proteins and caspases in the regulation of apoptosis (2011, background): “Apoptosis or PCD has conserved genetic and biochemical pathways [27, 101].”