ArticleJournal of molecular biology2012
Predictive Bcl-2 family binding models rooted in experiment or structure.
Article in Journal of molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 0 citations in OpenAlex.
- Article
- DDMut-PPI: predicting effects of mutations on protein-protein interactions using graph-based deep learning.Nucleic acids research · 2024Article
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- Surfaces: a software to quantify and visualize interactions within and between proteins and ligands.Bioinformatics (Oxford, England) · 2023Article
- Mutational scan inferred binding energetics and structure in intrinsically disordered protein CcdA.Protein science : a publication of the Protein Society · 2023Article
- Hypericin, a potential new BH3 mimetic.Frontiers in pharmacology · 2022Article
- Selective Affimers Recognise the BCL-2 Family Proteins BCL-xChembiochem : a European journal of chemical biology · 2021Article
- Tertiary Structural Motif Sequence Statistics Enable Facile Prediction and Design of Peptides that Bind Anti-apoptotic Bfl-1 and Mcl-1.Structure (London, England : 1993) · 2019Article
- Efficient flexible backbone protein-protein docking for challenging targets.Bioinformatics (Oxford, England) · 2018Article
- Article
- Computational design of self-assembling cyclic protein homo-oligomers.Nature chemistry · 2017Article
- Enriching Peptide Libraries for Binding Affinity and Specificity Through Computationally Directed Library Design.Methods in molecular biology (Clifton, N.J.) · 2017Article
- Computationally designed high specificity inhibitors delineate the roles of BCL2 family proteins in cancer.eLife · 2016Article
- Molecular Determinants of Mutant Phenotypes, Inferred from Saturation Mutagenesis Data.Molecular biology and evolution · 2016Article
- Designing helical peptide inhibitors of protein-protein interactions.Current opinion in structural biology · 2016Review
- Using Evolution to Guide Protein Engineering: The Devil IS in the Details.Biophysical journal · 2016Review
- AB-Bind: Antibody binding mutational database for computational affinity predictions.Protein science : a publication of the Protein Society · 2016Article
- Generating High-Accuracy Peptide-Binding Data in High Throughput with Yeast Surface Display and SORTCERY.Methods in molecular biology (Clifton, N.J.) · 2016Article
- Redefining the BH3 Death Domain as a 'Short Linear Motif'.Trends in biochemical sciences · 2015Review
- Locating Herpesvirus Bcl-2 Homologs in the Specificity Landscape of Anti-Apoptotic Bcl-2 Proteins.Journal of molecular biology · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Proteins of the Bcl-2 family either enhance or suppress programmed cell death and are centrally involved in cancer development and resistance to chemotherapy. BH3 (Bcl-2 homology 3)-only Bcl-2 proteins promote cell death by docking an α-helix into a hydrophobic groove on the surface of one or more of five pro-survival Bcl-2 receptor proteins. There is high structural homology within the pro-death and pro-survival families, yet a high degree of interaction specificity is nevertheless encoded, posing an interesting and important molecular recognition problem. Understanding protein features that dictate Bcl-2 interaction specificity is critical for designing peptide-based cancer therapeutics and diagnostics. In this study, we present peptide SPOT arrays and deep sequencing data from yeast display screening experiments that significantly expand the BH3 sequence space that has been experimentally tested for interaction with five human anti-apoptotic receptors. These data provide rich information about the determinants of Bcl-2 family specificity. To interpret and use the information, we constructed two simple data-based models that can predict affinity and specificity when evaluated on independent data sets within a limited sequence space. We also constructed a novel structure-based statistical potential, called STATIUM, which is remarkably good at predicting Bcl-2 affinity and specificity, especially considering it is not trained on experimental data. We compare the performance of our three models to each other and to alternative structure-based methods and discuss how such tools can guide prediction and design of new Bcl-2 family complexes.
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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 Socratic graph.