ArticleCommunications biology2023
Mutual induced-fit mechanism drives binding between intrinsically disordered Bim and cryptic binding site of Bcl-xL.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- Molecular recognition of natural compounds by MR1 and their implication in MAIT cell activation elucidated through McMD-based dynamic docking simulations.Scientific reports · 2025Article
- Allosteric regulation of BH3-in-groove interactions by tail anchors of BCL-xL complexes limits BH3 mimetic antagonism.Nature communications · 2025Article
- Binding Mechanism of Riboswitch to Natural Ligand Elucidated by McMD-Based Dynamic Docking Simulations.ACS omega · 2024Article
- Elucidation of binding mechanism, affinity, and complex structure between mWT1 tumor-associated antigen peptide and HLA-A*24:02.Protein science : a publication of the Protein Society · 2023Article
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intrinsically disordered region (IDR) of Bim binds to the flexible cryptic site of Bcl-xL, a pro-survival protein involved in cancer progression that plays an important role in initiating apoptosis. However, their binding mechanism has not yet been elucidated. We have applied our dynamic docking protocol, which correctly reproduced both the IDR properties of Bim and the native bound configuration, as well as suggesting other stable/meta-stable binding configurations and revealed the binding pathway. Although the cryptic site of Bcl-xL is predominantly in a closed conformation, initial binding of Bim in an encounter configuration leads to mutual induced-fit binding, where both molecules adapt to each other; Bcl-xL transitions to an open state as Bim folds from a disordered to an α-helical conformation while the two molecules bind each other. Finally, our data provides new avenues to develop novel drugs by targeting newly discovered stable conformations of Bcl-xL.
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