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Article: Nephrin deficiency activates NF-κB and promotes glomerular injury

TitleNephrin deficiency activates NF-κB and promotes glomerular injury
Authors
Issue Date2009
Citation
Journal of the American Society of Nephrology, 2009, v. 20 n. 8, p. 1733-1743 How to Cite?
AbstractIncreasing evidence implicates activation of NF-κB in a variety of glomerular diseases, but the mechanisms involved are unknown. Here, upregulation of NF-κB in the podocytes of transgenic mice resulted in glomerulosclerosis and proteinuria. Absence of the podocyte protein nephrin resulted in NF-κB activation, suggesting that nephrin negatively regulates the NF-κB pathway. Signal transduction assays supported a functional relationship between nephrin and NF-κB and suggested the involvement of atypical protein kinase C (aPKCζ/λ/ι) as an intermediary. We propose that disruption of the slit diaphragm leads to activation of NF-κB; subsequent upregulation of NF-κB-driven genes results in glomerular damage mediated by NF-κB-dependent pathways. In summary, nephrin may normally limit NF-κB activity in the podocyte, suggesting a mechanism by which it might discourage the evolution of glomerular disease. Copyright © 2009 by the American Society of Nephrology.
Persistent Identifierhttp://hdl.handle.net/10722/195476
ISSN
2015 Impact Factor: 8.491
2015 SCImago Journal Rankings: 4.699
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorHussain, S-
dc.contributor.authorRomio, L-
dc.contributor.authorSaleem, M-
dc.contributor.authorMathieson, P-
dc.contributor.authorSerrano, M-
dc.contributor.authorMoscat, J-
dc.contributor.authorDiaz-Meco, M-
dc.contributor.authorScambler, P-
dc.contributor.authorKoziell, A-
dc.date.accessioned2014-02-28T06:12:13Z-
dc.date.available2014-02-28T06:12:13Z-
dc.date.issued2009-
dc.identifier.citationJournal of the American Society of Nephrology, 2009, v. 20 n. 8, p. 1733-1743-
dc.identifier.issn1046-6673-
dc.identifier.urihttp://hdl.handle.net/10722/195476-
dc.description.abstractIncreasing evidence implicates activation of NF-κB in a variety of glomerular diseases, but the mechanisms involved are unknown. Here, upregulation of NF-κB in the podocytes of transgenic mice resulted in glomerulosclerosis and proteinuria. Absence of the podocyte protein nephrin resulted in NF-κB activation, suggesting that nephrin negatively regulates the NF-κB pathway. Signal transduction assays supported a functional relationship between nephrin and NF-κB and suggested the involvement of atypical protein kinase C (aPKCζ/λ/ι) as an intermediary. We propose that disruption of the slit diaphragm leads to activation of NF-κB; subsequent upregulation of NF-κB-driven genes results in glomerular damage mediated by NF-κB-dependent pathways. In summary, nephrin may normally limit NF-κB activity in the podocyte, suggesting a mechanism by which it might discourage the evolution of glomerular disease. Copyright © 2009 by the American Society of Nephrology.-
dc.languageeng-
dc.relation.ispartofJournal of the American Society of Nephrology-
dc.titleNephrin deficiency activates NF-κB and promotes glomerular injury-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1681/ASN.2008111219-
dc.identifier.pmid19497968-
dc.identifier.scopuseid_2-s2.0-68049120573-
dc.identifier.volume20-
dc.identifier.issue8-
dc.identifier.spage1733-
dc.identifier.epage1743-
dc.identifier.isiWOS:000268903200017-

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