Activation of PI3K, Akt, and ERK during early rotavirus infection leads to V-ATPase-dependent endosomal acidification required for uncoating
Soliman M, Seo J, Kim D, Kim J, Park J, Alfajaro M, Baek Y, Cho E, Kwon J, Choi J, Kang M, Park S, Cho K. Activation of PI3K, Akt, and ERK during early rotavirus infection leads to V-ATPase-dependent endosomal acidification required for uncoating. PLOS Pathogens 2018, 14: e1006820. PMID: 29352319, PMCID: PMC5792019, DOI: 10.1371/journal.ppat.1006820.Peer-Reviewed Original ResearchMeSH KeywordsAcidsAnimalsCaco-2 CellsCapsid ProteinsCattleCells, CulturedEndosomesEnzyme ActivationExtracellular Signal-Regulated MAP KinasesHaplorhiniHumansHydrogen-Ion ConcentrationPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRotavirusRotavirus InfectionsSf9 CellsSignal TransductionVacuolar Proton-Translocating ATPasesVirus UncoatingConceptsMEK/ERK pathwayV-ATPasePI3K/AktSubunit EOuter capsid proteinEndosomal acidificationLate endosomesERK pathwayCapsid proteinPI3KEarly infection eventsMEK/ERKCell surface receptorsImmunoprecipitation assaysPPI3KVirus traffickingProximity ligationMultistep bindingSurface receptorsAktViral progenyViral uncoatingERKRVA strainsEndosomes