Control of apoptosis by the BCL-2 protein family: implications for physiology and therapy

By P. Czabotar, G. Lessene, A. Strasser, Jerry M. Adams. Nature reviews. Molecular cell biology, 2013

3,023 citations recorded by the source corpus.

Subfields: Hepatology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c8dc166e429f64917a47f98e8bad9ef88df31c47

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Citations in the corpus

Mitochondria and Cancer (2016, background): “This cytochrome c release triggers the apoptosome and caspase protease activation in the cytosol, causing cell death (Figure 1) (Czabotar et al., 2014; Moldoveanu et al., 2014).”
MLKL compromises plasma membrane integrity by binding to phosphatidylinositol phosphates. (2014, background): “It is indeed conceivable that MLKL pore formation works similarly to the BH3-in groove Bcl-2 antagonist/killer and BAX homodimers, which upon activation, expose a hydrophobic surface that initiates HMW pore-forming structures (Czabotar et al., 2014).”
Lipotoxicity and the gut-liver axis in NASH pathogenesis. (2018, background): “4) comprises pivotal regulators of the mitochondrial outer membrane permeabilization [44].”
Broad targeting of resistance to apoptosis in cancer (2015, background): “However, there is evidence suggesting that Bcl-2 may play an oncogenic role through survival pathways other than its function at the mitochondrial membrane [11].”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “MOMP is antagonized by anti-apoptotic members of the BCL2 family, including BCL2 itself, BCL2 like 1 (BCL2L1; best known as BCL-XL), MCL1, BCL2 family apoptosis regulator (MCL1), BCL2 like 2 (BCL2L2; best known as BCL-W), and BCL2 related protein A1 (BCL2A1; best known—in human—as BFL-1) [29, 42, 43”
Synthetic Lethality of Combined Bcl-2 Inhibition and p53 Activation in AML: Mechanisms and Superior Antileukemic Efficacy (2017, background): “Anti-apoptotic Mcl-1 has been increasingly recognized as an important target in cancer therapy (Belmar and Fesik, 2015; Czabotar et al., 2014; Hata et al., 2015).”
Mitochondrial metabolism and cancer (2017, background): “, hypoxia, low nutrient availability, growth factor withdrawal), which would normally drive mitochondrial RCD via MOMP or MPT [32, 33].”
The design and development of covalent protein-protein interaction inhibitors for cancer treatment (2020, background): “Moreover, the inhibitor could target endogenous Grb2 and significantly inhibit mobility and viability in SK-BR-3 human breast cancer cells [95].”