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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Nuclear factor related to kappaB binding protein

NFRKB
Top mentioned proteins: HAD, FLI-1, NET, MLL, Ubiquitin
Papers on NFRKB
Expression Profiles of TGF-β and TLR Pathways in Porphyromonas gingivalis and Prevotella intermedia Challenged Osteoblasts.
New
Korachi et al., İstanbul, Turkey. In Jundishapur J Microbiol, Apr 2015
Amongst 48 genes examined, expressions of BMPER, SMAD1, IL8 and NFRKB were found to be highly upregulated by both bacterial challenges (Fold Change > 4).
Structural basis for the activation and inhibition of the UCH37 deubiquitylase.
New
Hill et al., Salt Lake City, United States. In Mol Cell, Apr 2015
We have performed biochemical characterization and determined crystal structures of UCH37 in complexes with RPN13 and NFRKB, which mediate its recruitment to the proteasome and INO80, respectively.
Systematic characterization of deubiquitylating enzymes for roles in maintaining genome integrity.
Impact
Jackson et al., Cambridge, United Kingdom. In Nat Cell Biol, 2014
Furthermore, we establish that the DUB UCHL5 regulates DSB resection and repair by homologous recombination through protecting its interactor, NFRKB, from degradation.
Proteome-wide discovery of mislocated proteins in cancer.
Lee et al., Suwŏn, South Korea. In Genome Res, 2013
The most common type of mislocation occurs between the endoplasmic reticulum and the nucleus; for example, for RNF138, TLX3, and NFRKB.
SNP array and phenotype correlation shows that FLI1 deletion per se is not responsible for thrombocytopenia development in Jacobsen syndrome.
Stejskal et al., Praha, Czech Republic. In Am J Med Genet A, 2012
The girl, who had a significantly longer deletion spanning all four genes suspected of being causative of JBS-related thrombocytopenia (FLI1, ETS1, NFRKB, and JAM3), did not manifest a platelet phenotype.
A common ancestry for BAP1 and Uch37 regulators.
Ponting et al., Oxford, United Kingdom. In Bioinformatics, 2012
This led to the discovery of two previously unrecognized domains in ASXL1: a forkhead (winged-helix) DNA-binding domain and a deubiquitinase adaptor domain shared with two regulators of ubiquitin carboxyl-terminal hydrolase 37 (Uch37), namely adhesion regulating molecule 1 (ADRM1) and nuclear factor related to kappaB (NFRKB).
Upregulation of nuclear factor-related kappa B suggests a disorder of transcriptional regulation in minimal change nephrotic syndrome.
GeneRIF
Sahali et al., Créteil, France. In Plos One, 2011
NFRKB may be involved in the disorders of transcriptional regulation commonly observed in minimal change nephrotic syndrome relapse.
Structure of a novel winged-helix like domain from human NFRKB protein.
Wilson et al., Los Angeles, United States. In Plos One, 2011
The human nuclear factor related to kappa-B-binding protein (NFRKB) is a 1299-residue protein that is a component of the metazoan INO80 complex involved in chromatin remodeling, transcription regulation, DNA replication and DNA repair.
Genetic dissection of granulomatous enterocolitis and arthritis in the intramural peptidoglycan-polysaccharide-treated rat model of IBD.
Mähler et al., Hannover, Germany. In Inflamm Bowel Dis, 2009
Possible candidate genes within these QTL (including Tnfrsf11a/RANK, Gpc5, Il2ra, and Nfrkb) are also implicated in the respective human diseases.
Second generation sequencing of the mesothelioma tumor genome.
Sugarbaker et al., Boston, United States. In Plos One, 2009
Additionally, three point mutations were observed in the coding regions of NKX6-2, a transcription regulator, and NFRKB, a DNA-binding protein involved in modulating NFKB1.
Submicroscopic deletions of 11q24-25 in individuals without Jacobsen syndrome: re-examination of the critical region by high-resolution array-CGH.
Rajcan-Separovic et al., Vancouver, Canada. In Mol Cytogenet, 2007
Their rearrangements facilitate the refinement of the JBS critical region and suggest that a) deletion of at least 3 of the 4 platelet function critical genes (ETS-1, FLI-1 and NFRKB and JAM3) is necessary for thrombocytopenia; b) one of the critical regions for heart abnormalities (conotruncal heart defects) may lie within 129.03 - 130.6 Mb; c) deletions of KCNJ1 and ADAMTS15 may contribute to the renal anomalies in Jacobsen Syndrome; d) the critical region for MRI abnormalities involves a region from 124.6 - 129.03 Mb.
Gene expression differences in normal esophageal mucosa associated with regression and progression of mild and moderate squamous dysplasia in a high-risk Chinese population.
Kirsch et al., Bethesda, United States. In Cancer Res, 2006
In contrast, individuals whose lesions progressed had higher expression of genes involved in immune suppression and inflammation (CNR2, NFATC4, NFRKB, MBP, INHBB, CMKLR1, CRP, ORMS, SERPINA7, and SERPINA1).
Amplified, lost, and fused genes in 11q23-25 amplicon in acute myeloid leukemia, an array-CGH study.
Knuutila et al., Helsinki, Finland. In Genes Chromosomes Cancer, 2006
Expression microarray of case 1 revealed that three of these genes, FLI1, NFRKB, and SNX19, were also overexpressed.
Girl with combined cellular immunodeficiency, pancytopenia, malformations, deletion 11q23.3 --> qter, and trisomy 8q24.3 --> qter.
Laidre et al., Tartu, Estonia. In Am J Med Genet, 2002
We are proposing that haploinsufficiency of the NFRKB gene on 11q24-q25 and/or the ETS-1 proto-oncogene on 11q24 may have caused or contributed to the immunodeficiency (decreased levels of B- and T-lymphocytes) in our patient.
Identification of amplified genes in a patient with acute myeloid leukemia and double minute chromosomes.
Morris et al., Christchurch, New Zealand. In Cancer Genet Cytogenet, 1999
Southern blot analysis confirmed the CGH findings and showed that the ETS1, FLI1, SRPR, NFRKB, and KCNJ5 genes located at 11q23-->24 were amplified, whereas the MLL at 11q23 was not amplified.
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