2022
Reovirus infection is regulated by NPC1 and endosomal cholesterol homeostasis
Ortega-Gonzalez P, Taylor G, Jangra RK, Tenorio R, Fernandez de Castro I, Mainou BA, Orchard RC, Wilen CB, Brigleb PH, Sojati J, Chandran K, Sachse M, Risco C, Dermody TS. Reovirus infection is regulated by NPC1 and endosomal cholesterol homeostasis. PLOS Pathogens 2022, 18: e1010322. PMID: 35263388, PMCID: PMC8906592, DOI: 10.1371/journal.ppat.1010322.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCholesterolEndosomesHomeostasisHumansMammalsNiemann-Pick C1 ProteinReoviridaeReoviridae InfectionsConceptsNiemann-Pick C1Cholesterol homeostasisActive reovirus core particlesRNA interference screenReovirus outer capsidInfectious subvirion particlesPutative host factorsReovirus infectionTreatment of cellsInterference screenMembrane proteinsEndocytic pathwayMammalian orthoreovirusGenome replicationLate endosomesEndosomal membranesPlasma membraneReovirus attachmentEndoplasmic reticulumOuter capsidViral transcriptionTransport activityEndosomesHomeostasisHuman immunodeficiency virus-1
2020
Intercellular Mitochondria Transfer to Macrophages Regulates White Adipose Tissue Homeostasis and Is Impaired in Obesity
Brestoff JR, Wilen CB, Moley JR, Li Y, Zou W, Malvin NP, Rowen MN, Saunders BT, Ma H, Mack MR, Hykes BL, Balce DR, Orvedahl A, Williams JW, Rohatgi N, Wang X, McAllaster MR, Handley SA, Kim BS, Doench JG, Zinselmeyer BH, Diamond MS, Virgin HW, Gelman AE, Teitelbaum SL. Intercellular Mitochondria Transfer to Macrophages Regulates White Adipose Tissue Homeostasis and Is Impaired in Obesity. Cell Metabolism 2020, 33: 270-282.e8. PMID: 33278339, PMCID: PMC7858234, DOI: 10.1016/j.cmet.2020.11.008.Peer-Reviewed Original ResearchConceptsIntercellular mitochondria transferMitochondria transferMitochondria uptakeMetabolic homeostasisGenome-wide CRISPRWhite adipose tissue homeostasisWAT macrophagesDistinct macrophage subpopulationsKnockout screensTissue homeostasisHeparan sulfateAdipose tissue homeostasisWhite adipose tissueGenes EXT1HomeostasisImmunometabolic crosstalkMitochondriaAdipocytesMyeloid cellsMacrophage subpopulationsCellsVivoRecent studiesMacrophagesCRISPR
2016
Homeostatic Control of Innate Lung Inflammation by Vici Syndrome Gene Epg5 and Additional Autophagy Genes Promotes Influenza Pathogenesis
Lu Q, Yokoyama CC, Williams JW, Baldridge MT, Jin X, DesRochers B, Bricker T, Wilen CB, Bagaitkar J, Loginicheva E, Sergushichev A, Kreamalmeyer D, Keller BC, Zhao Y, Kambal A, Green DR, Martinez J, Dinauer MC, Holtzman MJ, Crouch EC, Beatty W, Boon AC, Zhang H, Randolph GJ, Artyomov MN, Virgin HW. Homeostatic Control of Innate Lung Inflammation by Vici Syndrome Gene Epg5 and Additional Autophagy Genes Promotes Influenza Pathogenesis. Cell Host & Microbe 2016, 19: 102-113. PMID: 26764600, PMCID: PMC4714358, DOI: 10.1016/j.chom.2015.12.011.Peer-Reviewed Original ResearchConceptsAutophagy genesLung inflammationGene functionLethal influenza virus infectionBone marrow transplantation experimentsInnate immune inflammationInfluenza virus infectionEPG5Transplantation experimentsNormal homeostatic mechanismsHomeostatic controlInflammation supportLung transcriptomicsImmune inflammationRecurrent infectionsCytokine expressionInfluenza pathogenesisPulmonary abnormalitiesGenesInflammation resultsVirus infectionInfluenza resistanceElevated baselineHomeostatic mechanismsLung physiology