Showing 61 - 80 results of 196 for search 'app sequence model', query time: 0.09s Refine Results
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    TransBind allows precise detection of DNA-binding proteins and residues using language models and deep learning by Md Toki Tahmid, A.K.M. Mehedi Hasan, Md Shamsuzzoha Bayzid

    Published 2025-04-01
    “…To address these challenges, we introduce TransBind, an alignment-free deep learning framework that predicts DNA-binding proteins and residues directly from a single primary sequence, eliminating the need for MSAs. By leveraging features from pre-trained protein language models, TransBind effectively handles the issue of data imbalance and achieves superior performance. …”
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    Uncovering Social States in Healthy and Clinical Populations Using Digital Phenotyping and Hidden Markov Models: Observational Study by Imogen E Leaning, Andrea Costanzo, Raj Jagesar, Lianne M Reus, Pieter Jelle Visser, Martien J H Kas, Christian F Beckmann, Henricus G Ruhé, Andre F Marquand

    Published 2025-04-01
    “…We trained the HMM on a subset of HCs (91/348, 26.1%) and selected a model with socially active and inactive states. Then, we generated hidden state sequences per participant and calculated their “total dwell time,” that is, the percentage of time spent in the socially active state. …”
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    Mutations in hnRNP A1 drive neurodegeneration and alternative RNA splicing of neuronal gene targets by Ansalna Ansari, Patricia A. Thibault, Hannah E. Salapa, Joseph-Patrick W.E. Clarke, Michael C. Levin

    Published 2025-03-01
    “…Herein, we utilized a novel, neuron-specific model of neurodegeneration by transducing primary mouse neurons with mutant forms of the RNA binding protein heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) identified from MS patients, including one within the M9-nuclear localization sequence of hnRNP A1 (A1(P275S)) and a second in the prion-like domain of hnRNP A1 (A1(F263S)) to test the hypothesis that neuronal hnRNP A1 dysfunction drives neurodegeneration in MS.Examination of hnRNP A1 localization in neurons revealed an increase in nucleocytoplasmic mislocalization in neurons transduced with A1(P275S), but not A1(F263S). …”
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