@article{SCOPUS_ID:105029446962,

title = {Honokiol blocks tumor development and metastasis through mitochondrion-targeted effects},

author = {Martina Grandi and Francesco Boldrin and Giovanni Risato and Silvia Grillini and Natascia Tiso and Francesco Argenton and Emanuela Leonardi and Silvio Tosatto and Giancarlo Solaini and Alessandra Baracca and Valentina Giorgio},

url = {https://www.scopus.com/record/display.uri?eid=2-s2.0-105029446962&origin=inward},

doi = {10.1038/s41419-026-08441-6},

year  = {2026},

date = {2026-01-01},

journal = {Cell Death and Disease},

volume = {17},

number = {1},

publisher = {Springer Nature},

abstract = {© The Author(s) 2026.IF1 is the natural inhibitor of the mitochondrial ATP synthase during hydrolytic activity. It has been found to be overexpressed in many tumors, where it acts as a pro-oncogenic protein. During oxidative phosphorylation, IF1 binds to a novel site on the OSCP subunit of ATP synthase and promotes tumorigenesis by protecting cancer cells from permeability transition pore (PTP)-dependent apoptosis. In this work, honokiol, a biphenolic compound, showed binding affinity for two sites on the OSCP subunit, as predicted by molecular docking analysis. It was shown to be effective in disrupting the IF1-OSCP interaction and sensitizing cancer cells to apoptosis. In vivo, xenografts of zebrafish injected with IF1-expressing HeLa cells showed tumor development. The same xenografts, treated with honokiol, showed a significant reduction in tumor mass, similar to untreated fish injected with IF1 KO HeLa cells. In vitro, honokiol inhibits colony formation in soft agar of IF1-expressing HeLa cells by promoting the PTP opening and cell death, without any effect on cell proliferation. Interestingly, honokiol was shown to block metastasis in fish xenografts and migration in a wound healing assay, by promoting mitochondrial swelling in both control and IF1 KO cell lines, when cells are moving to close the scratch area. In conclusion, honokiol appears to be a promising anti-cancer compound, with pro-apoptotic properties through the displacement of IF1 from the OSCP subunit of ATP synthase, and anti-metastatic effects that are due to mitochondrial PTP opening.},

note = {Cited by: 1; Open Access},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{SCOPUS_ID:105028199071,

title = {Early multimodal behavioral cues in autism: a micro-analytical exploration of actions, gestures and speech during naturalistic parent-child interactions},

author = {Mastrogiuseppe and Famà and Bruschetta and Leonardi and Campisi and Aiello and Carrozza and Ruggeri and Baieli and Campisi and Turriziani and Di Rosa and Lombardo and Tartarisco and Capirci and Pioggia and Ruta},

url = {https://www.scopus.com/record/display.uri?eid=2-s2.0-105028199071&origin=inward},

doi = {10.1016/j.ijchp.2026.100664},

year  = {2026},

date = {2026-01-01},

journal = {International Journal of Clinical and Health Psychology},

volume = {26},

number = {1},

publisher = {Elsevier B.V.},

abstract = {© 2026 The Author(s).Early signs of autism often emerge through distinct developmental pathways, particularly in communication, social interaction, and play. While naturalistic parent-child interactions during free play are ideal for observing spontaneous social behaviors, few autism studies have adopted this ecological and developmental approach. To address this gap, we used a fine-grained microanalytic method to examine motor, gestural, and vocal behaviors in young children, integrating machine learning to explore how combinations of these traits distinguish early autistic neurodivergence. We analyzed video recordings of 58 autistic and non-autistic children (aged 13–40 months) engaged in naturalistic parent-child play. A frame-by-frame micro-coding scheme was applied to capture actions, gestures, speech, and their multimodal integration. Clear differences emerged between neurotypical (NT) and autistic (ASC) children. NT children displayed more gestures, particularly deictic and conventional-interactive, greater gesture–gaze coordination, more functional object play, and more frequent multi-word utterances. In contrast, ASC children showed fewer deictic and conventional-interactive gestures and greater use of instrumental gestures, reduced gesture–gaze coordination, a higher reliance on vocalizations rather than words, and increased object manipulation compared to functional play. Feature selection using ANOVA F-tests identified a core set of key predictors most frequently and independently selected across folds of cross-validation: Alternate Gaze, Reaching, and Instrumental Gesture. Higher values of Alternate Gaze were associated with NT classification, while elevated frequencies of Reaching and Instrumental Gestures were linked to ASC classification. A logistic regression classifier trained on these features achieved over 85% accuracy in distinguishing the two groups. These findings underscore the value of an ecologically valid, and developmentally informed approach to identifying early behavioral markers of autism, supporting earlier recognition and the design of more personalized, strengths-based interventions.},

note = {Cited by: 0; Open Access},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{SCOPUS_ID:105033505349,

title = {Exploring proteins and protein–ligand complexes through residue interaction networks},

author = {Sol C. Begue and Emanuela Leonardi and Giovanni Minervini and Silvio C. E. Tosatto},

url = {https://www.scopus.com/record/display.uri?eid=2-s2.0-105033505349&origin=inward},

doi = {10.1038/s41596-026-01334-0},

year  = {2026},

date = {2026-01-01},

journal = {Nature Protocols},

publisher = {Springer Nature},

abstract = {© Springer Nature Limited 2026.Protein structures provide a wealth of information regarding biological functions and underlying mechanisms. The growing availability of high-quality structure predictions and extended molecular simulations has further expanded the potential to leverage these data in a myriad of different ways. Yet, an abundance of data can obscure important information, making it difficult to focus on biologically relevant features. Residue interaction networks (RINs) address this challenge by condensing structural data into subsets of well-defined noncovalent molecular interactions. In this Protocol, we explore how the RIN generator (RING) software can be used to gain biological insights by constructing detailed RINs for proteins and protein–ligand complexes. We provide a step-by-step guide to performing both single- and multi-state protein analyses using the RING web server and a stand-alone software package. In addition, we include a dedicated procedure for sequential multi-file analysis, which can be performed exclusively through the command-line interface. All potential inputs and outputs are explained in detail, along with strategies for downstream data processing. Designed for researchers in biology and related fields with minimal or no programming experience, the entire workflow can be completed in <45 min.},

note = {Cited by: 0},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{SCOPUS_ID:105027748200,

title = {DisProt in 2026: enhancing intrinsically disordered proteins accessibility, deposition, and annotation},

author = {Maria Victoria Nugnes and Kamel Eddine Adel Bouhraoua and Mehdi Zoubiri and Rita Pancsa and Erzsébet Fichó and Alexander M Monzon and Ana M Melo and Edoardo Salladini and Emanuela Leonardi and Federica Quaglia and Daniyal Nasiribavil and Hamidreza Ghafouri and Gobeill Julien and Emilie Pasche and Patrick Ruch and Paul Van Rijen and László Dobson and Marco Schiavina and Trinidad Cordero and Zsófia E Kálmán and Ximena Castro and Valentín Iglesias and István Reményi and Mahta Mehdiabadi and Gábor Erdős and Zsuzsanna Dosztányi and Peter Tompa and Damiano Piovesan and Silvio C. E Tosatto and Maria Cristina Aspromonte},

url = {https://www.scopus.com/record/display.uri?eid=2-s2.0-105027748200&origin=inward},

doi = {10.1093/nar/gkaf1175},

year  = {2026},

date = {2026-01-01},

journal = {Nucleic Acids Research},

volume = {54},

number = {D1},

pages = {D383-D392},

publisher = {Oxford University Press},

abstract = {© 2025 The Author(s). Published by Oxford University Press.DisProt (https://disprot.org/) is an open database integrating experimental evidence on intrinsically disordered proteins (IDPs), intrinsically disordered regions (IDRs), and their functions. Over the past two years, the database has grown over 20%, now comprising 3201 IDPs and 13 347 pieces of evidence, including over 1500 new structural state annotations and >1300 new function annotations. DisProt has systematically adopted the Minimum Information About Disorder Experiments (MIADE) guidelines, more than doubling annotations with experimental details and improving the interpretability of disorder-related experiments. The website has evolved into a hybrid knowledgebase and deposition system, introducing a Deposition Page that allows direct submissions by external users. Through BLAST-based homology propagation in MobiDB, DisProt disorder regions and linear interacting peptides have been extended from hundreds to hundreds of thousands of proteins across >11 000 organisms. This new release marks a paradigm shift by integrating computational predictions as valid evidence and introducing major updates and restructuring of the IDP Ontology, enhancing accuracy, interoperability, and semantic clarity. DisProt continues to support community engagement through training resources together with DisTriage, an AI-based literature triage tool, providing curators with regularly updated lists of prioritized publications.},

note = {Cited by: 4; Open Access},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

@article{SCOPUS_ID:86000084600,

title = {Genetic variants and phenotypic data curated for the CAGI6 intellectual disability panel challenge},

author = {Maria Cristina Aspromonte and Alessio Del Conte and Roberta Polli and Demetrio Baldo and Francesco Benedicenti and Elisa Bettella and Stefania Bigoni and Stefania Boni and Claudia Ciaccio and Stefano D’Arrigo and Ilaria Donati and Elisa Granocchio and Isabella Mammi and Donatella Milani and Susanna Negrin and Margherita Nosadini and Fiorenza Soli and Franco Stanzial and Licia Turolla and Damiano Piovesan and Silvio C. E. Tosatto and Alessandra Murgia and Emanuela Leonardi},

url = {https://www.scopus.com/record/display.uri?eid=2-s2.0-86000084600&origin=inward},

doi = {10.1007/s00439-025-02733-1},

year  = {2025},

date = {2025-01-01},

journal = {Human Genetics},

volume = {144},

number = {2},

pages = {309-326},

publisher = {Springer Science and Business Media Deutschland GmbH},

abstract = {© The Author(s) 2025.Neurodevelopmental disorders (NDDs) are common conditions including clinically diverse and genetically heterogeneous diseases, such as intellectual disability, autism spectrum disorders, and epilepsy. The intricate genetic underpinnings of NDDs pose a formidable challenge, given their multifaceted genetic architecture and heterogeneous clinical presentations. This work delves into the intricate interplay between genetic variants and phenotypic manifestations in neurodevelopmental disorders, presenting a dataset curated for the Critical Assessment of Genome Interpretation (CAGI6) ID Panel Challenge. The CAGI6 competition serves as a platform for evaluating the efficacy of computational methods in predicting phenotypic outcomes from genetic data. In this study, a targeted gene panel sequencing has been used to investigate the genetic causes of NDDs in a cohort of 415 paediatric patients. We identified 60 pathogenic and 49 likely pathogenic variants in 102 individuals that accounted for 25% of NDD cases in the cohort. The most mutated genes were ANKRD11, MECP2, ARID1B, ASH1L, CHD8, KDM5C, MED12 and PTCHD1 The majority of pathogenic variants were de novo, with some inherited from mildly affected parents. Loss-of-function variants were the most common type of pathogenic variant. In silico analysis tools were used to assess the potential impact of variants on splicing and structural/functional effects of missense variants. The study highlights the challenges in variant interpretation especially in cases with atypical phenotypic manifestations. Overall, this study provides valuable insights into the genetic causes of NDDs and emphasises the importance of understanding the underlying genetic factors for accurate diagnosis, and intervention development in neurodevelopmental conditions.},

note = {Cited by: 4; Open Access},

keywords = {},

pubstate = {published},

tppubtype = {article}

}