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Interactions between proteins and nucleic acids are at the heart of many essential biological processes. Despite increasing structural information about how these interactions may take place, our understanding of the usage made of protein surfaces by nucleic acids is still very limited. This is in part due to the inherent complexity associated to protein surface deformability and evolution. In this work, we present a method that contributes to decipher such complexity by predicting protein-DNA interfaces and characterizing their properties. It relies on three biologically and physically meaningful descriptors, namely evolutionary conservation, physico-chemical properties and surface geometry. We carefully assessed its performance on several hundreds of protein structures and compared it to several machine-learning state-of-the-art methods. Our approach achieves a higher sensitivity compared to the other methods, with a similar precision. Importantly, we show that it is able to unravel 'hidden' binding sites by applying it to unbound protein structures and to proteins binding to DNA via multiple sites and in different conformations. It is also applicable to the detection of RNA-binding sites, without significant loss of performance. This confirms that DNA and RNA-binding sites share similar properties. Our method is implemented as a fully automated tool, [Formula: see text], freely accessible at: http://www.lcqb.upmc.fr/JET2DNA. We also provide a new dataset of 187 protein-DNA complex structures, along with a subset of 82 associated unbound structures. The set represents the largest body of high-resolution crystallographic structures of protein-DNA complexes, use biological protein assemblies as DNA-binding units, and covers all major types of protein-DNA interactions. It is available at: http://www.lcqb.upmc.fr/PDNAbenchmarks.
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http://dx.doi.org/10.1371/journal.pcbi.1007624 | DOI Listing |
ACS Nano
September 2025
State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing 100191, China.
Nanoparticles bind to proteins in cells selectively and form a protein corona around them. However, the mechanisms of protein conformational changes underlying the interactions between nanoparticles and protein coronas remain poorly understood. In this study, we prepared small molecule self-assembled nanoparticles (Aloin NPs) as a research tool to investigate the allosteric mechanism of protein coronas.
View Article and Find Full Text PDFThe ratio of nonsynonymous (d ) to synonymous (d ) substitutions in protein-coding genes is a fundamental metric in molecular evolution to test hypotheses about the relative contributions of genetic drift and natural selection in shaping patterns of protein divergence (Williams et al., 2020). However, interpretation of d /d ratios may be confounded by sequence context and specific substitution models (Hughes, 2007; Kryazhimskiy & Plotkin, 2008).
View Article and Find Full Text PDFUnlabelled: Kaposi's sarcoma-associated herpesvirus (KSHV) orchestrates late gene transcription through viral transcriptional activators that hijack host RNA polymerase II machinery, maintaining selectivity for viral promoters. Among these, the KSHV protein ORF24 serves as a TATA-binding protein (TBP) mimic essential for recognizing viral late promoters, although the molecular mechanisms underlying its function remain poorly characterized. Here, we used AlphaFold3 to predict the structure of ORF24 in complex with DNA and validated key features in both transfected cells and during KSHV lytic replication.
View Article and Find Full Text PDFProgrammable DNA integration using CRISPR-associated transposons (CASTs) offers powerful capabilities for genome engineering. The single effector Cas12k CAST examples evolved from a fixed guide TnpB nuclease protein. Here, we engineer de novo RNA-guided transposition systems, where the single guide RNA effector components are repurposed nuclease-dead TnpB-family proteins.
View Article and Find Full Text PDFInvest New Drugs
September 2025
Departamento de Química and Institute for Advanced Research in Chemical Science (IAdChem), Facultad de Ciencias, Universidad Autónoma de Madrid, Módulo 13, 28049, Madrid, Spain.
The oncogenic transcription factor MYC drives proliferation, metabolism, and therapy resistance in the majority of human cancers, yet its large, nuclear protein-protein interface has long frustrated direct drug discovery. A pivotal breakthrough was the identification of Tribbles pseudokinase 3 (TRIB3) as a high-affinity scaffold that binds the helix-loop-helix/leucine zipper region of MYC, blocks the E3-ubiquitin-ligase, UBE3B, from tagging critical lysines, and thereby prolongs MYC protein half-life while enhancing MYC-MAX transcriptional output. This review integrates structural, biochemical, and in vivo data to show how genetic deletion or pharmacological eviction of TRIB3 collapses MYC levels, silences its gene program, and suppresses tumor growth in B-cell lymphomas and selected solid tumors.
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