Control of mitochondrial apoptosis by the Bcl-2 family
By J. Brunelle, A. Letai. Journal of Cell Science, 2009
917 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/68ad8f048d9855fd2bc81a2b2d1022f23db92d9e
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Citations in the corpus
- Apoptosis as anticancer mechanism: function and dysfunction of its modulators and targeted therapeutic strategies (2016, background): “The pro-apoptotic BH3-only proteins act upstream of this event binding with high affinity to anti-apoptotic Bcl-2 family members thereby allowing Bax/Bak to elicit MOMP and activation of the caspase cascade [36,37].”
- Anti-apoptosis and cell survival: a review. (2011, background): “An up-regulation of autophagy is also unlikely to be responsible for the antagonist effects of other anti-apoptotic processes such as the ability of Bcl2 to directly interfere with the pro-apoptotic function of activated Bax [10].”
- Role of Bcl-2 family proteins and caspases in the regulation of apoptosis (2011, background): “Following death signal, BH3 domain-only proteins also known as minimal death domain can neutralize or depress antiapoptotic Bcl-2 proteins allowing pro-apoptotic proteins such as Bax/Bak-like proteins to induce apoptosis [39, 40].”