2025
TNFRSF1A and NCF1 May Act as Hub Genes in Mastitis
Ekhtiyari M, Yousefi M, Samadian F, Ghaderi‐Zefrehei M, Neysi S, Shamsabadi J, Javanmard A, Shahriarpour H, Lesch B. TNFRSF1A and NCF1 May Act as Hub Genes in Mastitis. Veterinary Medicine And Science 2025, 11: e70278. PMID: 40028770, PMCID: PMC11875065, DOI: 10.1002/vms3.70278.Peer-Reviewed Original ResearchConceptsBovine mastitisHub genesMastitis susceptibilityExpression datasetsMolecular mechanismsMultiple expression datasetsProtein-protein interactionsCo-expression network analysisSusceptibility to bovine mastitisRegulatory networksTarget key genesKey genesDairy industryMolecular playersNetwork analysisMRNA-miRNACo-expressionGenesNCF1MastitisBacterial infectionsTherapeutic targetTNFRSF1AImmune responseSusceptibilityMultifaceted analysis of noncoding and coding de novo variants implicates NOTCH signaling pathway in tetralogy of Fallot in Chinese population
Lin Q, Zhang D, Gruber P, Tam P, Lui V, Wu Z, Hong H, Chien K, Sham P, Tang C. Multifaceted analysis of noncoding and coding de novo variants implicates NOTCH signaling pathway in tetralogy of Fallot in Chinese population. Human Genetics And Genomics Advances 2025, 6: 100414. PMID: 39921258, PMCID: PMC11910093, DOI: 10.1016/j.xhgg.2025.100414.Peer-Reviewed Original ResearchPediatric Cardiac Genomics ConsortiumProtein-protein interactionsNoncoding variantsCoding de novo variantsNotch signalingPopulation genetic heterogeneityEvidence of genetic contributionEtiology of TOFDysregulated gene expressionNotch signaling pathwayNotch signaling genesDysregulation of Notch signalingChinese populationTetralogy of FallotCyanotic heart defectsCandidate genesOutflow tract morphogenesisGenetic heterogeneitySignaling GenesGenomics ConsortiumBioinformatics analysisGene expressionCo-expressionGenetic contributionSignaling pathway
2024
Representing core gene expression activity relationships using the latent structure implicit in Bayesian networks
Gao J, Gerstein M. Representing core gene expression activity relationships using the latent structure implicit in Bayesian networks. Bioinformatics 2024, 40: btae463. PMID: 39051682, PMCID: PMC11316617, DOI: 10.1093/bioinformatics/btae463.Peer-Reviewed Original ResearchTranscriptional regulatory networksGene regulatory networksCo-expression networkGene expression activityChIP-seqGene conservationCluster genesSupplementary dataRegulatory networksBiological networksClearer clusteringCo-expressionExpression activityBioinformaticsGenesBiomedical studiesConservationExpressionClustersMapping the influence of hydrocarbons mixture on molecular mechanisms, involved in breast and lung neoplasms: in silico toxicogenomic data-mining
Abu-Bakar A, Ismail M, Zulkifli M, Zaini N, Shukor N, Harun S, Inayat-Hussain S. Mapping the influence of hydrocarbons mixture on molecular mechanisms, involved in breast and lung neoplasms: in silico toxicogenomic data-mining. Genes And Environment 2024, 46: 15. PMID: 38982523, PMCID: PMC11232146, DOI: 10.1186/s41021-024-00310-y.Peer-Reviewed Original ResearchNon-apoptotic programmed cell deathSignaling pathwayMolecular mechanismsResponse to oxidative stressInterleukin-17 signaling pathwayMolecular pathwaysSurvival signaling pathwaysAdaptive response to oxidative stressOxidative stress responseBreast cancer invasionGenetic interactionsModulate IL-8Protein domainsCytoscape softwareAir pollutionCritical genesCell deathCo-expressionGenesRisk of breastStress responseToxicogenomic analysisToxicogenomics toolsDevelopment of breastInvestigated hydrocarbonsCritical reasoning on the co-expression module QTL in the dorsolateral prefrontal cortex
Cote A, Young H, Huckins L. Critical reasoning on the co-expression module QTL in the dorsolateral prefrontal cortex. Human Genetics And Genomics Advances 2024, 5: 100311. PMID: 38773772, PMCID: PMC11214266, DOI: 10.1016/j.xhgg.2024.100311.Peer-Reviewed Original ResearchConceptsExpression quantitative trait lociGene co-expressionCo-expressionExpression quantitative trait locus methodGenetic variantsComplex trait heritabilityMultiple testing burdenGene-based testsQuantitative trait lociTrans-eQTLsCis-eQTLsRegulatory variationSequencing datasetsTrait lociGene regulationTrait heritabilityGene functionGene modulesReal-data applicationModule genesGenesTesting burdenDorsolateral prefrontal cortexVariantsComparison to prior studiesMitofusin 2 plays a critical role in maintaining the functional integrity of the neuromuscular-skeletal axis
Zhu M, Zeiss C, Hamrick M, Weinstein R, Sun B, Brotto M, Liu X, Siu E, Huttner A, Tommasini S, Simpson C, Insogna K. Mitofusin 2 plays a critical role in maintaining the functional integrity of the neuromuscular-skeletal axis. Bone 2024, 184: 117086. PMID: 38552893, DOI: 10.1016/j.bone.2024.117086.Peer-Reviewed Original ResearchConceptsDeletion of Mfn2Bone mineral densityMitofusin 2Reduced expression of Mfn2Myofiber atrophySpinal cordTransgenic mice expressing CreMice expressing CreNon-redundant roleSkeletal muscle histologyLumbar spinal cordTrabecular bone massLean body massExpression of Mfn2Mitochondrial reticulumMFN2 geneDisruption of cellular architectureImpaired osteoblast differentiationOsteoblast lineage commitmentMfn2Mitochondrial sizeMitofusinMineral densityCo-expressionDisorganized sarcomeres
2023
Senataxin helicase, the causal gene defect in ALS4, is a significant modifier of C9orf72 ALS G4C2 and arginine-containing dipeptide repeat toxicity
Bennett C, Dastidar S, Arnold F, McKinstry S, Stockford C, Freibaum B, Sopher B, Wu M, Seidner G, Joiner W, Taylor J, West R, La Spada A. Senataxin helicase, the causal gene defect in ALS4, is a significant modifier of C9orf72 ALS G4C2 and arginine-containing dipeptide repeat toxicity. Acta Neuropathologica Communications 2023, 11: 164. PMID: 37845749, PMCID: PMC10580588, DOI: 10.1186/s40478-023-01665-z.Peer-Reviewed Original ResearchConceptsDipeptide repeatsFamilial amyotrophic lateral sclerosisAmyotrophic lateral sclerosisRNA-protein interactionsC9orf72 amyotrophic lateral sclerosisMobility of proteinsNuclear helicaseRNA-dependentDrosophila modelFly linesSenataxin functionFly modelCellular processesC9orf72 geneMembraneless organellesGenetic modifiersSenataxinMovement assayGenetic causeCo-expressionPrimary neuronsDisease phenotypeSporadic amyotrophic lateral sclerosisAge-related motor deficitsHEK293 cells
2022
Double knockin mice show NF-κB trajectories in immune signaling and aging
Rahman S, Aqdas M, Martin E, Ardori F, Songkiatisak P, Oh K, Uderhardt S, Yun S, Claybourne Q, McDevitt R, Greco V, Germain R, Tessarollo L, Sung M. Double knockin mice show NF-κB trajectories in immune signaling and aging. Cell Reports 2022, 41: 111682. PMID: 36417863, PMCID: PMC9764224, DOI: 10.1016/j.celrep.2022.111682.Peer-Reviewed Original Research
2017
Single-cell analysis of CCR6+ human Th cells reveals varying degrees of the type-17 phenotype, ranging from cells co-expressing to those fully suppressing opposing pathways
Singh S, Edara N, Zhang H, Chen J, Farber J. Single-cell analysis of CCR6+ human Th cells reveals varying degrees of the type-17 phenotype, ranging from cells co-expressing to those fully suppressing opposing pathways. The Journal Of Immunology 2017, 198: 150.14-150.14. DOI: 10.4049/jimmunol.198.supp.150.14.Peer-Reviewed Original ResearchType 17Co-expressionLineage-specific genesCo-expressed genesCells expressing various levelsTh cellsExpression of genesPattern of expressionSingle-cell analysisExpression of CCR6Opposing pathwaysMulti-lineage cellsGenesHuman Th cellsCells co-expressingLineagesDifferentiation in vivoCell sortingCCR6 expressionExpression levelsMemory populationIL-22IL-17A/FRT-PCRCCR6
2015
The PIAS-like Coactivator Zmiz1 Is a Direct and Selective Cofactor of Notch1 in T Cell Development and Leukemia
Pinnell N, Yan R, Cho H, Keeley T, Murai M, Liu Y, Alarcon A, Qin J, Wang Q, Kuick R, Elenitoba-Johnson K, Maillard I, Samuelson L, Cierpicki T, Chiang M. The PIAS-like Coactivator Zmiz1 Is a Direct and Selective Cofactor of Notch1 in T Cell Development and Leukemia. Immunity 2015, 43: 870-883. PMID: 26522984, PMCID: PMC4654973, DOI: 10.1016/j.immuni.2015.10.007.Peer-Reviewed Original ResearchConceptsT cell developmentIntestinal homeostasisNotch target genesT-ALLT-cell acute lymphoblastic leukemiaCell acute lymphoblastic leukemiaZMIZ1Pan-Notch inhibitorsTarget genesAcute lymphoblastic leukemiaCell developmentTumor suppressorCo-expressionNotch signalingActive Notch1Promote cancerMyeloid suppressionLymphoblastic leukemiaNotch1Leukemic growthNotch inhibitorClinical trialsHomeostasisLeukemiaInhibitors
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