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dc.creatorCaster, Dawn J. 
dc.creatorKorte, Erik A. 
dc.creatorNanda, Sambit K. 
dc.creatorMcLeish, Kenneth R. 
dc.creatorOliver, Rebecca K. 
dc.creatorG'Sell, Rachel T. 
dc.creatorSheehan, Ryan M. 
dc.creatorFreeman, Darrell W. 
dc.creatorCoventry, Susan C. 
dc.creatorKelly, Jennifer A. 
dc.creatorGuthridge, Joel M. 
dc.creatorJames, Judith A. 
dc.creatorSivils, Kathy L. 
dc.creatorAlarcon-Riquelme, Marta E. 
dc.creatorScofield, R. Hal 
dc.creatorAdrianto, Indra 
dc.creatorGaffney, Patrick M. 
dc.creatorStevens, Anne M. 
dc.creatorFreedman, Barry I. 
dc.creatorLangefeld, Carl D. 
dc.creatorTsao, Betty P. 
dc.creatorPons-Estel, Bernardo A. 
dc.creatorJacob, Chaim O. 
dc.creatorKamen, Diane L. 
dc.creatorGilkeson, Gary S. 
dc.creatorBrown, Elizabeth E. 
dc.creatorAlarcon, Graciela S. 
dc.creatorEdberg, Jeffrey C. 
dc.creatorKimberly, Robert P. 
dc.creatorMartin, Javier 
dc.creatorMerrill, Joan T. 
dc.creatorHarley, John B. 
dc.creatorKaufman, Kenneth M. 
dc.creatorReveille, John D. 
dc.creatorAnaya, Juan-Manuel 
dc.creatorCriswell, Lindsey A. 
dc.creatorVila, Luis M. 
dc.creatorPetri, Michelle 
dc.creatorRamsey-Goldman, Rosalind 
dc.creatorBae, Sang-Cheol 
dc.creatorBoackle, Susan A. 
dc.creatorVyse, Timothy J. 
dc.creatorNiewold, Timothy B. 
dc.creatorCohen, Philip 
dc.creatorPowell, David W. 
dc.date.accessioned2020-05-25T23:56:39Z
dc.date.available2020-05-25T23:56:39Z
dc.date.created2013
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/22476
dc.description.abstract"The genetic factors underlying the pathogenesis of lupus nephritis associated with systemic lupus erythematosus are largely unknown, although animal studies indicate that nuclear factor (NF)-?B is involved. We reported previously that aknockin mouse expressinganin active form of ABIN1 (ABIN1[D485N]) develops lupus-like autoimmune disease and demonstrates enhanced activation of NF-?B and mitogen-activated protein kinases in immune cells after toll-like receptor stimulation. In the current study, we show that ABIN1[D485N] mice develop progressive GN similar to class III and IV lupus nephritis in humans. To investigate the clinical relevance of ABIN1 dysfunction, we genotyped five single-nucleotide polymorphisms in the gene encoding ABIN1, TNIP1, in samples from European-American, African American, Asian, Gullah, and Hispanic participants in the Large Lupus Association Study 2. Comparing cases of systemic lupus erythematosus with nephritis and cases ofsystemic lupus erythematosus without nephritis revealed strong associations with lupus nephritis at rs7708392 in European Americans and rs4958881 in African Americans. Comparing cases of systemic lupus erythematosus with nephritis and healthy controls revealed a stronger association at rs7708392 in European Americans but not at rs4958881 in African Americans. Our data suggest that variants in the TNIP1 gene are associated with the risk for lupus nephritis and could be mechanistically involved in disease development via aberrant regulation of NF-?B and mitogen-activated protein kinase activity. Copyright © 2013 by the American Society of Nephrology."
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.relation.ispartofJournal of the American Society of Nephrology, Vol.24, No.11 (2013); pp. 1743-1754
dc.relation.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-84887052296&doi=10.1681%2fASN.2013020148&partnerID=40&md5=92a52685140adacf0d756894c60962df
dc.sourceinstname:Universidad del Rosario
dc.sourcereponame:Repositorio Institucional EdocUR
dc.titleABIN1 dysfunction as a genetic basis for lupus nephritis
dc.typearticle
dc.subject.keywordImmunoglobulin enhancer binding protein
dc.subject.keywordMitogen activated protein kinase
dc.subject.keywordsingle nucleotide
dc.subject.keywordinbred c57bl
dc.subject.keywordknockout
dc.subject.keywordToll like receptor
dc.subject.keywordA20 binding inhibitor of immunoglobulin enhancer binding protein 1 gene
dc.subject.keywordAfrican american
dc.subject.keywordAnimal experiment
dc.subject.keywordAnimal model
dc.subject.keywordArticle
dc.subject.keywordControlled study
dc.subject.keywordEuropean american
dc.subject.keywordGene
dc.subject.keywordGenotype
dc.subject.keywordImmunocompetent cell
dc.subject.keywordLupus erythematosus nephritis
dc.subject.keywordMouse
dc.subject.keywordNonhuman
dc.subject.keywordPathophysiology
dc.subject.keywordPriority journal
dc.subject.keywordSingle nucleotide polymorphism
dc.subject.keywordSystemic lupus erythematosus
dc.subject.keywordAnimals
dc.subject.keywordDna-binding proteins
dc.subject.keywordFluorescent antibody technique
dc.subject.keywordHumans
dc.subject.keywordKidney
dc.subject.keywordLupus nephritis
dc.subject.keywordMice
dc.subject.keywordMice
dc.subject.keywordMice
dc.subject.keywordNf-kappa b
dc.subject.keywordPolymorphism
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.type.spaArtículo
dc.rights.accesoAbierto (Texto Completo)
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.identifier.doihttps://doi.org/10.1681/ASN.2013020148
dc.relation.citationEndPage1754
dc.relation.citationIssueNo. 11
dc.relation.citationStartPage1743
dc.relation.citationTitleJournal of the American Society of Nephrology
dc.relation.citationVolumeVol. 24


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