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Upregulation of nuclear factor-related kappa B suggests a disorder of transcriptional regulation in minimal change nephrotic syndrome.

Immune mechanisms underlying the pathophysiology of idiopathic nephrotic syndrome, the most frequent glomerular disease in children, are believed to involve a systemic disorder of T cell function and cell mediated immunity. How these perturbations take place remains unclear. We report here that NFRK... Full description

Journal Title: PloS one 2012, Vol.7(1), p.e30523
Main Author: Audard, Vincent
Other Authors: Pawlak, André , Candelier, Marina , Lang, Philippe , Sahali, Djillali
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0030523
Link: http://search.proquest.com/docview/919227858/?pq-origsite=primo
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title: Upregulation of nuclear factor-related kappa B suggests a disorder of transcriptional regulation in minimal change nephrotic syndrome.
format: Article
creator:
  • Audard, Vincent
  • Pawlak, André
  • Candelier, Marina
  • Lang, Philippe
  • Sahali, Djillali
subjects:
  • Adolescent–Genetics
  • Adult–Isolation & Purification
  • Cloning, Molecular–Metabolism
  • DNA-Binding Proteins–Physiology
  • Gene Expression Regulation–Physiology
  • Genetic Predisposition to Disease–Genetics
  • Hek293 Cells–Metabolism
  • Humans–Pathology
  • Jurkat Cells–Genetics
  • Middle Aged–Genetics
  • Nephrosis, Lipoid–Genetics
  • Protein Processing, Post-Translational–Genetics
  • Recurrence–Genetics
  • Transcription, Genetic–Genetics
  • Up-Regulation–Genetics
  • Young Adult–Genetics
  • DNA-Binding Proteins
  • Nfrkb Protein, Human
ispartof: PloS one, 2012, Vol.7(1), p.e30523
description: Immune mechanisms underlying the pathophysiology of idiopathic nephrotic syndrome, the most frequent glomerular disease in children, are believed to involve a systemic disorder of T cell function and cell mediated immunity. How these perturbations take place remains unclear. We report here that NFRKB, a member of the chromatin remodeling complex, is upregulated in MCNS relapse, mainly in CD4+T cells and B cells and undergo post-translational modifications including sumoylation. We showed that NFRKB was highly expressed in nuclear compartment during the relapse, while it was restricted to cytoplasm in remission. NFRKB induced the activation of AP1 signaling pathway by upregulating the expression of c-jun. We showed that NFRKB promotes hypomethylation of genomic DNA, suggesting its implication in regulation of gene expression by enhancing the binding of transcription factors through chromatin remodeling. These results suggest for the first time that NFRKB may be involved in the disorders of transcriptional regulation commonly observed in MCNS relapse.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0030523
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titleUpregulation of nuclear factor-related kappa B suggests a disorder of transcriptional regulation in minimal change nephrotic syndrome.
creatorAudard, Vincent ; Pawlak, André ; Candelier, Marina ; Lang, Philippe ; Sahali, Djillali
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identifierE-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0030523
subjectAdolescent–Genetics ; Adult–Isolation & Purification ; Cloning, Molecular–Metabolism ; DNA-Binding Proteins–Physiology ; Gene Expression Regulation–Physiology ; Genetic Predisposition to Disease–Genetics ; Hek293 Cells–Metabolism ; Humans–Pathology ; Jurkat Cells–Genetics ; Middle Aged–Genetics ; Nephrosis, Lipoid–Genetics ; Protein Processing, Post-Translational–Genetics ; Recurrence–Genetics ; Transcription, Genetic–Genetics ; Up-Regulation–Genetics ; Young Adult–Genetics ; DNA-Binding Proteins ; Nfrkb Protein, Human
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descriptionImmune mechanisms underlying the pathophysiology of idiopathic nephrotic syndrome, the most frequent glomerular disease in children, are believed to involve a systemic disorder of T cell function and cell mediated immunity. How these perturbations take place remains unclear. We report here that NFRKB, a member of the chromatin remodeling complex, is upregulated in MCNS relapse, mainly in CD4+T cells and B cells and undergo post-translational modifications including sumoylation. We showed that NFRKB was highly expressed in nuclear compartment during the relapse, while it was restricted to cytoplasm in remission. NFRKB induced the activation of AP1 signaling pathway by upregulating the expression of c-jun. We showed that NFRKB promotes hypomethylation of genomic DNA, suggesting its implication in regulation of gene expression by enhancing the binding of transcription factors through chromatin remodeling. These results suggest for the first time that NFRKB may be involved in the disorders of transcriptional regulation commonly observed in MCNS relapse.
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