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Fan Liu

Publications and source records attributed to Fan Liu.

3 recordsLinked to original sources
PubMed2026

Structure-resolved virus-host interactomics by cross-linking mass spectrometry.

Viruses depend on host protein networks to replicate, assemble progeny, and spread between cells and organisms. Defining these virus-host protein interactions is challenging because they are highly dependent on infection stage, cell type, species, and because mechanistic interpretation requires information about structural interfaces and conformational states. Cross-linking mass spectrometry (XL-MS) addresses these challenges by adding a spatial and structural dimension to virus-host interactomics in native systems. In this review, we discuss how XL-MS has advanced from targeted analysis of viral protein complexes to structure-resolved mapping of virion architecture and infected-cell virus-host interactomes. We highlight how XL-MS complements AP-MS, cryo-EM/cryo-ET, quantitative proteomics, genetic perturbation, and structure prediction to connect physical proximity with molecular mechanisms. Finally, we discuss current limitations in sensitivity, chemical coverage, temporal resolution, and model interpretation, and outline how future quantitative and integrative XL-MS workflows may enable systems-level structural virology.

Mass Spectrometry↗
PubMed2025

ToxAssay: a hierarchical model-driven tool for advanced toxicogenomics biomarker discovery.

MOTIVATION: Understanding the genetic basis of drug-induced toxicity is crucial for drug development. In-silico analysis of toxicogenomics datasets facilitates early detection of toxicity biomarkers. However, existing tools struggle with the complex interdependencies among hierarchically structured variables, leading to inaccurate biomarker identification. To address this limitation, we developed a Hierarchical Linear Model (HLM) and implemented it in the R package ToxAssay, offering extensive functionality for comprehensive toxicity assessment. RESULTS: ToxAssay outperforms existing methods by improving biomarker detection and computational efficiency. Applied to glutathione depletion-induced toxicity, it prioritized 71 key genes and identified 26 core genes with high discriminative accuracy (AUC = 0.97) and strong cross-correlation (Pearson's r = 0.88) with external datasets. Additionally, our advance outcome pathway (AOP) analysis algorithm uncovered disease outcomes linked to glutathione depletion. These findings provide precise insights into the molecular mechanisms driving drug-induced toxicity. AVAILABILITY AND IMPLEMENTATION: ToxAssay is available as an open-source R package at https://github.com/Fun-Gene/toxassay.

Biomarkers↗
PubMed2025

Inactivation of β-1,3-glucan synthase-like 5 confers broad-spectrum resistance to Plasmodiophora brassicae pathotypes in cruciferous plants.

Clubroot disease, caused by the obligate intracellular rhizarian protist Plasmodiophora brassicae, is devastating to cruciferous crops worldwide. Widespread field P. brassicae pathotypes frequently overcome the pathotype-specific resistance of modern varieties, posing a challenge for durable control of this disease. Here a genome-wide association study of 3 years of data comprising field clubroot phenotyping of 244 genome-resequenced Brassica napus accessions identified a strong association of β-1,3-glucan synthase-like 5 (GSL5) with clubroot susceptibility. GSL5 was evolutionarily conserved, and inactivation of GSL5 by genome editing in Arabidopsis, B. napus, Brassica rapa and Brassica oleracea conferred broad-spectrum, high-level resistance to P. brassicae pathotypes without yield penalties in B. napus. GSL5 inactivation derepressed the jasmonic acid-mediated immunity during P. brassicae secondary infection, and this immune repression was possibly reinforced through stabilization of GSL5 by a P. brassicae effector, facilitating clubroot susceptibility. Our study provides durable resistance resources for cruciferous clubroot disease control and insights into plant resistance against intracellular eukaryotic phytopathogens.

Disease Resistance↗