2012
Human spliceosomal protein CWC22 plays a role in coupling splicing to exon junction complex deposition and nonsense-mediated decay
Alexandrov A, Colognori D, Shu MD, Steitz JA. Human spliceosomal protein CWC22 plays a role in coupling splicing to exon junction complex deposition and nonsense-mediated decay. Proceedings Of The National Academy Of Sciences Of The United States Of America 2012, 109: 21313-21318. PMID: 23236153, PMCID: PMC3535618, DOI: 10.1073/pnas.1219725110.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceCarrier ProteinsEukaryotic Initiation Factor-4AEukaryotic Initiation Factor-4GExonsGene Knockdown TechniquesHEK293 CellsHeLa CellsHumansMolecular Sequence DataMutationNonsense Mediated mRNA DecayNuclear ProteinsPeptidylprolyl IsomeraseProtein BindingRNA SplicingRNA, MessengerRNA-Binding ProteinsSpliceosomesConceptsExon junction complexEJC depositionMultiprotein exon junction complexNonsense-mediated decay pathwayNonsense-mediated decaySpecific roleEJC assemblyEJC formationComplex eukaryotesDisrupts associationMetazoan mRNAsSpliceosomal proteinsCellular mRNAsHost genesSplicing defectsJunction complexDownstream eventsSplicingNatural substrateDecay pathwaysCWC22Depletion yieldsNMDMutationsMRNA
2011
Human eIF4AIII interacts with an eIF4G-like partner, NOM1, revealing an evolutionarily conserved function outside the exon junction complex
Alexandrov A, Colognori D, Steitz JA. Human eIF4AIII interacts with an eIF4G-like partner, NOM1, revealing an evolutionarily conserved function outside the exon junction complex. Genes & Development 2011, 25: 1078-1090. PMID: 21576267, PMCID: PMC3093123, DOI: 10.1101/gad.2045411.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsDEAD-box RNA HelicasesEukaryotic Initiation Factor-4AEukaryotic Initiation Factor-4GEvolution, MolecularExonsGene DeletionGenetic Complementation TestHumansModels, MolecularMolecular Sequence DataMutationNuclear ProteinsPhenotypeProtein Structure, TertiaryRNA, Ribosomal, 18SRNA-Binding ProteinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSequence AlignmentConceptsExon junction complexEIF4GJunction complexDEAD-box helicasePre-rRNA processingDirect physical interactionEIF4G complexExtragenic suppressorsBiogenesis defectsLethal phenotypeGrowth defectTranslation initiationHuman orthologEIF4AIIISaccharomyces cerevisiaeHuman cellsNOM1Physical interactionComplex actsG complexX-ray structureMutationsResiduesComplexesOrthologs
2010
miR-29 and miR-30 regulate B-Myb expression during cellular senescence
Martinez I, Cazalla D, Almstead LL, Steitz JA, DiMaio D. miR-29 and miR-30 regulate B-Myb expression during cellular senescence. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 108: 522-527. PMID: 21187425, PMCID: PMC3021067, DOI: 10.1073/pnas.1017346108.Peer-Reviewed Original ResearchConceptsB-myb expressionCellular senescenceMiR-30MiR-29Reporter constructsEndogenous B-MybMajor tumor suppressor mechanismTumor suppressor mechanismIrreversible growth arrestMicroRNA familiesMutant 3'UTRCellular DNA synthesisB-MybReplicative senescenceCompensatory mutationsGrowth arrestMutant sitesRb pathwaySenescenceSuppressor mechanismDNA synthesisRepressionInhibits senescenceExpressionMutations
1993
Mutations in the conserved loop of human U5 snRNA generate use of novel cryptic 5′ splice sites in vivo.
Cortes JJ, Sontheimer EJ, Seiwert SD, Steitz JA. Mutations in the conserved loop of human U5 snRNA generate use of novel cryptic 5′ splice sites in vivo. The EMBO Journal 1993, 12: 5181-5189. PMID: 8262061, PMCID: PMC413781, DOI: 10.1002/j.1460-2075.1993.tb06213.x.Peer-Reviewed Original ResearchConceptsSplice siteRabbit beta-globin geneBeta-globin transcriptsBeta-globin geneU5 genesConserved loopMRNA splicingU5 snRNASecond intronFirst exonExon sequencesLoop mutantsSecond exonExpression vectorTransient transfectionCryptic sitesNovel siteHeLa cellsGT dinucleotideExonsExon 1U5 sequencesSnRNAMutationsVivo system