ArticlePloS one2012
Upregulation of nuclear factor-related kappa B suggests a disorder of transcriptional regulation in minimal change nephrotic syndrome.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed.
- Toll-like receptor 3 expression and function in childhood idiopathic nephrotic syndrome.Clinical and experimental immunology · 2015Trial
- Neuronal Injury and Regeneration-Linked Gene Expression Dynamics in the Hypothalamic-Pituitary-Adrenal Axis Following Experimental Traumatic Brain Injury.International journal of molecular sciences · 2026Article
- Gene Expression as a Guide to the Development of Novel Therapies in Primary Glomerular Diseases.Journal of clinical medicine · 2021Article
- Rituximab Induces Complete Remission of Proteinuria in a Patient With Minimal Change Disease and No Detectable B Cells.Frontiers in immunology · 2020Article
- [Minimal change disease and focal segmental glomerulosclerosis].Der Internist · 2019Review
- Changes in DNA methylation in naïve T helper cells regulate the pathophysiological state in minimal-change nephrotic syndrome.BMC research notes · 2017Article
- The Calcium-Induced Regulation in the Molecular and Transcriptional Circuitry of Human Inflammatory Response and Autoimmunity.Frontiers in pharmacology · 2017Article
- Minimal change disease and idiopathic FSGS: manifestations of the same disease.Nature reviews. Nephrology · 2016Review
- Pathogenesis of minimal change nephrotic syndrome: an immunological concept.Korean journal of pediatrics · 2016Review
- [New insight in pathogenesis of podocyte disfunction in minimal change disease].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2016Article
- Cell biology and genetics of minimal change disease.F1000Research · 2016Review
- Role of the glucocorticoid receptor in the recurrence of primary nephrotic syndrome.Experimental and therapeutic medicine · 2015Article
- Prevalence of herpesviruses at onset of idiopathic nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2014Article
- Protection Effect of Zhen-Wu-Tang on Adriamycin-Induced Nephrotic Syndrome via Inhibiting Oxidative Lesions and Inflammation Damage.Evidence-based complementary and alternative medicine : eCAM · 2014Article
- DNA methylation changes between relapse and remission of minimal change nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.