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Biology subjects

Borisek, J.

Publications and source records attributed to Borisek, J..

2 recordsLinked to original sources

BATTLE-AMP: Benchmarking Antimicrobial Peptide Predictors

As antimicrobial resistance outpaces antibiotic development, antimicrobial peptides (AMPs) have emerged as a promising class of alternative antibacterials, and computational predictors are increasingly used to prioritize AMP candidates. Such predictors are typically evaluated on binary AMP/non-AMP classification, which does not test whether they can identify peptides with clinically relevant potency against specific pathogens. We present BATTLE-AMP, a benchmarking framework that evaluates AMP predictors against experimentally measured minimum inhibitory concentrations (MICs) across clinically relevant bacterial species and strains. We surveyed 48 published methods, finding fewer than 25% reproducible, and benchmarked 10 model families (21 variants) using experimental MIC data, synthetic sequence perturbations, activity cliff analyses, and all-atom molecular dynamics (MD) simulations. Four findings emerge: (i) models trained on MIC data outperform binary classifiers regardless of architecture; (ii) the best model depends on the target pathogen, so model selection must be guided by the biological question; (iii) most models cannot distinguish active peptides from inactive sequences with identical amino acid composition; and (iv) activity cliffs remain unresolved by both machine learning and MD, marking a limit of current computational methods. BATTLE-AMP is released as an open Snakemake framework at https://github.com/szczurek-lab/battleamp-snakemake for benchmarking new models and scoring novel candidate libraries.

bioinformatics↗

Allosteric Cross-Talk Among SARS-CoV-2 Spike's Receptor-Binding Domain Mutations Triggers an Effective Hijacking of Human Cell Receptor

The rapid and relentless emergence of novel highly transmissible SARS-CoV-2 variants, possibly decreasing vaccine efficacy, currently represents a formidable medical and societal challenge. These variants frequently hold mutations on the Spike proteins Receptor-Binding Domain (RBD), which, binding to the Angiotensin-Converting Enzyme 2 (ACE2) receptor, mediates viral entry into the host cells. Here, all-atom Molecular Dynamics simulations and Dynamical Network Theory of the wild-type and mutant RBD/ACE2 adducts disclose that while the N501Y mutation (UK variant) enhances the Spikes binding affinity towards ACE2, the N501Y, E484K and K417N mutations (South African variant) aptly adapt to increase SARS-CoV-2 propagation via a two-pronged strategy: (i) effectively grasping ACE2 through an allosteric signaling between pivotal RBD structural elements; and (ii) impairing the binding of antibodies elicited by infected/vaccinated patients. This information, unlocking the molecular terms and evolutionary strategies underlying the increased virulence of emerging SARS-CoV-2 variants, set the basis for developing the next-generation anti-COVID-19 therapeutics. TOC GRAPHICS O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=174 SRC="FIGDIR/small/441093v1_ufig1.gif" ALT="Figure 1"> View larger version (71K): org.highwire.dtl.DTLVardef@107419aorg.highwire.dtl.DTLVardef@163fc8eorg.highwire.dtl.DTLVardef@159eb0borg.highwire.dtl.DTLVardef@5621eb_HPS_FORMAT_FIGEXP M_FIG C_FIG

biophysics↗