Differential targeting of prosurvival Bcl-2 proteins by their BH3-only ligands allows complementary apoptotic function.

By Lin Chen, Simon N. Willis, A. Wei, Brian J. Smith, J. Fletcher, M. G. Hinds, P. Colman, C. Day, Jerry M. Adams, D. Huang. Molecules and Cells, 2005

1,894 citations recorded by the source corpus.

Subfields: Computational Theory and Mathematics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e13f9b4fbcf5a68d59864128cede2ce381981bb5

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In Computational Theory and Mathematics

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In Molecular Biology

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Citations in the corpus

• Control of mitochondrial apoptosis by the Bcl-2 family (2009, background): “Each anti-apoptotic protein has its own pattern of interaction with sensitizer proteins (Certo et al., 2006; Chen et al., 2005; Kuwana et al., 2005; Opferman et al., 2003).”
• Caspase-independent cell death (2005, background): “Recent studies indicate that BH3-only proteins fall into two subfamilies: those that can directly trigger opening of the Bax-Bak channel to precipitate MOMP, and those that sensitize for opening of the latter channel by neutralizing members of the Bcl-2 family that can inhibit channel openin”
• Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “Different BH3-only proteins have been suggested to preferentially bind specific anti-apoptotic BCL2 family members (e.g., BID, BIM, and PUMA potently bind all anti-apoptotic BCL2 family members; BAD preferentially interacts with BCL2, BCL-XL, and BCL-W; NOXA preferentially inhibits MCL1; and HRK pre”
• BCL-2 family antagonists for cancer therapy (2008, background): “Selective interactions of the BH3-only proteins with pro-survival proteins are now well documente”
• Tumor resistance to apoptosis (2009, background): “The direct activation model holds that BH3-only proteins, which act as direct activators such as Bim and the cleaved form of Bid (tBid), bind directly to Bax and Bak to trigger their activation, whereas BH3-only proteins that act as sensitizers, e.g., Bad, bind to the pro-survival Bcl-2 proteins.51 ”
• BCL-2 family proteins: changing partners in the dance towards death (2017, background): “Adding to the confusion, different peptide lengths are often used for BH3only proteins within the same paper.(24,25) Generally, BH3 peptide length correlates with increased affinity for the binding partner suggesting that residues outside of the BH3 domain facilitate proper interactions among BCL-2 ”
• The Bcl-2 apoptotic switch in cancer development and therapy (2007, background): “Importantly, the promiscuous binders (e.g. Bim and Puma) are much more potent killers than those that cannot engage all the pro-survival proteins, but the combination of Noxa and Bad potently induces cell death (Figure 2b; Chen et al., 2005).”
• Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “In contrast, the indirect activation model proposes that BH3-only proteins activate Bax and Bak in an indirect manner by binding to the multiple anti-apoptotic Bcl-2 proteins that inhibit Bax and Bak, which in turn leads to the release of Bax and Bak [33, 34].”
• The BH3 mimetic ABT-737 targets selective Bcl-2 proteins and efficiently induces apoptosis via Bak/Bax if Mcl-1 is neutralized. (2006, methodology): “ABT-737, a Bad-like BH3 mimetic compound In contrast to these compounds, in solution competition assays (Chen et al., 2005) the BH3 mimetic ABT-737 (Oltersdorf et al.”
• How do BCL-2 proteins induce mitochondrial outer membrane permeabilization? (2008, neutral): “Also, the majority of data concerning the interactions between BH3only protein and anti-apoptotic members is based on synthetic BH3 domain peptides and their interaction with immobilized, recombinant anti-apoptotic proteins by Biacore analysis or overexpression [ 15 ,18].”
• Neuronal Cell Death. (2018, positive): “It is clear that different BH3-only proteins display selective binding to anti-apoptotic Bcl-2 family members (104, 344, 373).”
• EGFR-TKI resistance due to BIM polymorphism can be circumvented in combination with HDAC inhibition. (2013, background): “Gene products (such as BIMEL, BIML, and BIMS) with a BH3 domain, which is essential for apoptosis induction, antagonize antiapoptotic proteins (such as Bcl-2, Bcl-XL, and Mcl-1) and activate proapoptotic proteins (such as BAX and BAK), thereby inducing apoptosis (6, 7).”