ArticleeLife2016
Computationally designed high specificity inhibitors delineate the roles of BCL2 family proteins in cancer.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 87 citations in OpenAlex.
- Article
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- Screening of the Prodiginine Molecules as BH3-mimetics against the Developed Bcl-2 Antiapoptotic Chemotherapeutic Resistance: A Molecular Docking and ADMET Study Supported by Molecular Dynamics Simulations.Current computer-aided drug design · 2026Article
- Breaking Boundaries in Cancer Therapy: Harnessing Chromothripsisinduced Mutations for Targeted Bcl-2 Protein Destabilization.Current drug discovery technologies · 2026Article
- Multiplex design and discovery of proximity handles for programmable proteome editing.bioRxiv : the preprint server for biology · 2025Article
- Molecular mechanisms underlying HRK interaction with BCL-XL and BCL-2 reveal specificity determinants for BH3 mimetics.iScience · 2025Article
- Computational design of potent and selective binders of BAK and BAX.Science advances · 2025Article
- Grafted Coiled-Coil Peptides as Multivalent Scaffolds for Protein Recognition.ACS chemical biology · 2025Article
- Intracellular delivery of proteins for live cell imaging.Journal of controlled release : official journal of the Controlled Release Society · 2025Article
- The impact of curation errors in the PDBBind Database on machine learning predictions of protein-protein binding affinity.Database : the journal of biological databases and curation · 2025Article
- Computational Modeling of Chromoanagenesis- or Chromothripsis-Induced SNPs in Antiapoptotic Genes: Their Impact on Protein Structure and Function.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Accurate de novo design of heterochiral protein-protein interactions.Cell research · 2024Article
- Soybean β-Conglycinin and Cowpea β-Vignin Peptides Inhibit Breast and Prostate Cancer Cell Growth: An In Silico and In Vitro Approach.Foods (Basel, Switzerland) · 2024Article
- Massively parallel measurement of protein-protein interactions by sequencing using MP3-seq.Nature chemical biology · 2024Article
- De novo design of mini-protein binders broadly neutralizing Clostridioides difficile toxin B variants.Nature communications · 2024Article
- Article
- Ergodicity Breaking and Self-Destruction of Cancer Cells by Induced Genome Chaos.Entropy (Basel, Switzerland) · 2023Article
- Anti-proliferative activity, molecular genetics, docking analysis, and computational calculations of uracil cellulosic aldehyde derivatives.Scientific reports · 2023Article
- A dataset comprised of binding interactions for 104,972 antibodies against a SARS-CoV-2 peptide.Scientific data · 2022Article
- Computational design of an apoptogenic protein that binds BCL-xL and MCL-1 simultaneously and potently.Computational and structural biotechnology journal · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
Abstract
Many cancers overexpress one or more of the six human pro-survival BCL2 family proteins to evade apoptosis. To determine which BCL2 protein or proteins block apoptosis in different cancers, we computationally designed three-helix bundle protein inhibitors specific for each BCL2 pro-survival protein. Following in vitro optimization, each inhibitor binds its target with high picomolar to low nanomolar affinity and at least 300-fold specificity. Expression of the designed inhibitors in human cancer cell lines revealed unique dependencies on BCL2 proteins for survival which could not be inferred from other BCL2 profiling methods. Our results show that designed inhibitors can be generated for each member of a closely-knit protein family to probe the importance of specific protein-protein interactions in complex biological processes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.