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Gabriel Monteiro da Silva

Publications and source records attributed to Gabriel Monteiro da Silva.

3 recordsLinked to original sources

Pearl: A Foundation Model for Placing Every Atom in the Right Location

Accurately predicting the three-dimensional structures of protein-ligand complexes remains a fundamental challenge in computational drug discovery that limits the pace and success of therapeutic design. Deep learning methods have recently shown strong potential as structural prediction tools, achieving promising accuracy across diverse biomolecular systems. However, their performance and utility are constrained by scarce experimental data, inefficient architectures, physically invalid poses, and the limited ability to exploit auxiliary information available at inference. To address these issues, we introduce Pearl (Placing Every Atom in the Right Location), a foundation model for protein-ligand cofolding at scale. Pearl addresses these challenges with three key innovations: (1) training recipes that include large-scale synthetic data to overcome data scarcity; (2) architectures that incorporate an SO(3)-equivariant diffusion module to inherently respect 3D rotational symmetries, improving generalization and sample efficiency, and (3) controllable inference, including a generalized multi-chain templating system supporting both protein and non-polymeric components as well as dual unconditional/conditional modes. Pearl establishes a new state-of-the-art performance in protein-ligand cofolding. On the key metric of generating accurate (RMSD < 2 Å) and physically valid poses, Pearl surpasses AlphaFold 3 and other open source baselines on the public Runs N' Poses and PoseBusters benchmarks, delivering 14.5% and 14.2% improvements, respectively, over the next best model. In the pocket-conditional cofolding regime, Pearl delivers $3.6\times$ improvement on a proprietary set of challenging, real-world drug targets at the more rigorous RMSD < 1 Å threshold. Finally, we demonstrate that model performance correlates directly with synthetic dataset size used in training.

cs.LG↗

Compound Mutations in the Abl1 Kinase Cause Inhibitor Resistance by Shifting DFG Flip Mechanisms and Relative State Populations

The intrinsic dynamics of most proteins are central to their function. Protein tyrosine kinases such as Abl1 undergo significant conformational changes that modulate their activity in response to different stimuli. These conformational changes constitute a conserved mechanism for self-regulation that dramatically impacts kinases' affinities for inhibitors. Few studies have attempted to extensively sample the pathways and elucidate the mechanisms that underlie kinase inactivation. Seeking to bridge this knowledge gap, we present a thorough analysis of the ``DFG flip'' inactivation pathway in Abl1 kinase. By leveraging the power of the Weighted Ensemble methodology, which accelerates sampling without the use of biasing forces, we have comprehensively simulated DFG flip events in Abl1 and its inhibitor-resistant variants, revealing a rugged landscape punctuated by potentially druggable intermediate states. Through our strategy, we successfully simulated dozens of uncorrelated DFG flip events distributed along two principal pathways, identified the molecular mechanisms that govern them, and measured their relative probabilities. Further, we show that the compound Glu255Lys/Val Thr315Ile Abl1 variants owe their inhibitor resistance phenotype to an increase in the free energy barrier associated with completing the DFG flip. This barrier stabilizes Abl1 variants in conformations that can lead to loss of binding for Type-II inhibitors such as Imatinib or Ponatinib. Finally, we contrast our Abl1 observations with the relative state distributions and propensity for undergoing a DFG flip of evolutionarily-related protein tyrosine kinases with diverging Type-II inhibitor binding affinities. Altogether, we expect that our work will be of significant importance for protein tyrosine kinase inhibitor discovery.

physics.bio-ph↗

Predicting Relative Populations of Protein Conformations without a Physics Engine Using AlphaFold2

This paper presents a novel approach for predicting the relative populations of protein conformations using AlphaFold 2, an AI-powered method that has revolutionized biology by enabling the accurate prediction of protein structures. While AlphaFold 2 has shown exceptional accuracy and speed, it is designed to predict proteins' single ground state conformations and is limited in its ability to predict fold switching and the effects of mutations on conformational landscapes. Here, we demonstrate how AlphaFold 2 can directly predict the relative populations of different conformations of proteins and even accurately predict changes in those populations induced by mutations by subsampling multiple sequence alignments. We tested our method against NMR experiments on two proteins with drastically different amounts of available sequence data, Abl1 kinase and the granulocyte-macrophage colony-stimulating factor, and predicted changes in their relative state populations with accuracies in excess of 80%. Our method offers a fast and cost-effective way to predict protein conformations and their relative populations at even single point mutation resolution, making it a useful tool for pharmacology, analyzing NMR data, and studying the effects of evolution.

physics.bio-ph↗