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Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, epsilon

IkappaBepsilon, NFKBIE
The protein encoded by this gene binds to components of NF-kappa-B, trapping the complex in the cytoplasm and preventing it from activating genes in the nucleus. Phosphorylation of the encoded protein targets it for destruction by the ubiquitin pathway, which activates NF-kappa-B by making it available to translocate to the nucleus. [provided by RefSeq, Sep 2011] (from NCBI)
Top mentioned proteins: NF-kappaB, IkappaBalpha, IkappaBbeta, p65, Rel
Papers on IkappaBepsilon
Impaired NFKBIE gene function decreases cellular uptake of methotrexate by down-regulating SLC19A1 expression in a human rheumatoid arthritis cell line.
Mitani et al., Tokyo, Japan. In Mod Rheumatol, Feb 2016
OBJECTIVE: A non-synonymous single nucleotide polymorphism (nsSNP, rs2233434, Val194Ala) in the NFKBIE (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, epsilon) gene is known to be a rheumatoid arthritis (RA) susceptibility polymorphism in the Japanese RA population and could be closely associated with nuclear factor kappaB (NF-κB) activity.
Whole-exome sequencing in relapsing chronic lymphocytic leukemia: clinical impact of recurrent RPS15 mutations.
Rosenquist et al., Uppsala, Sweden. In Blood, Jan 2016
In addition to mutations with known adverse-prognostic impact (TP53, NOTCH1, ATM, SF3B1, NFKBIE, BIRC3) a large proportion of cases (19.5%) harbored mutations in RPS15, a gene encoding a component of the 40S ribosomal subunit.
Genetic landscapes of relapsed and refractory diffuse large B cell lymphomas.
Johnson et al., Vancouver, Canada. In Clin Cancer Res, Jan 2016
We observed individual examples of clonal expansions affecting genes whose mutations had not been previously associated with DLBCL including two regulators of NF-κB: NFKBIE and NFKBIZ.
Exome sequencing of desmoplastic melanoma identifies recurrent NFKBIE promoter mutations and diverse activating mutations in the MAPK pathway.
Bastian et al., San Francisco, United States. In Nat Genet, Oct 2015
Newly identified alterations included recurrent promoter mutations of NFKBIE, encoding NF-κB inhibitor ɛ (IκBɛ), in 14.5% of samples.
Functional loss of IκBε leads to NF-κB deregulation in aggressive chronic lymphocytic leukemia.
Rosenquist et al., Uppsala, Sweden. In J Exp Med, Jul 2015
The most frequently mutated gene was NFKBIE (21/315 cases; 7%), which encodes IκBε, a negative regulator of NF-κB in normal B cells.
Network-assisted analysis of primary Sjögren's syndrome GWAS data in Han Chinese.
Wang et al., Beijing, China. In Sci Rep, 2014
Of these pSS candidates, 14 genes had been reported to be associated with any of pSS, RA, and SLE, including STAT4, GTF2I, HLA-DPB1, HLA-DRB1, PTTG1, HLA-DQB1, MBL2, TAP2, CFLAR, NFKBIE, HLA-DRA, APOM, HLA-DQA2 and NOTCH4.
Systematic Genome-wide Screening and Prediction of microRNAs in EBOV During the 2014 Ebolavirus Outbreak.
Cao et al., Beijing, China. In Sci Rep, 2014
Combing bioinformatics analysis and prediction of the potential ebolavirus miRNA target genes, we suggest that two ebolavirus coding possible miRNAs may be silence and down-regulate the target genes NFKBIE and RIPK1, which are the central mediator of the pathways related with host cell defense mechanism.
Acquired initiating mutations in early hematopoietic cells of CLL patients.
Bernard et al., Tokyo, Japan. In Cancer Discov, 2014
NFKBIE and EGR2 mutations were observed at unexpectedly high frequencies, 10.7% and 8.3% of 168 advanced-stage patients, respectively.
Focussed microarray analysis of apoptosis in periodontitis and its potential pharmacological targeting by carvacrol.
Uitto et al., Porto Alegre, Brazil. In Arch Oral Biol, 2014
Forty-nine out of 70 genes from this model, such as CSF2RB, NFKBIE, ENDOG, CASP10 and CASP3, were differentially expressed (corrected p-value<0.05) in periodontitis samples when compared to those of healthy controls.
6p21.2-p12.3 deletion detected by aCGH in an 8-year-old girl with cleidocranial dysplasia and developmental delay.
Wang et al., Taipei, Taiwan. In Gene, 2013
We discuss the genotype-phenotype correlation and the consequence of haploinsufficiency of CUL7, VEGFA, NFKBIE and RUNX2 in this case.
PADI4 and HLA-DRB1 are genetic risks for radiographic progression in RA patients, independent of ACPA status: results from the IORRA cohort study.
Momohara et al., Tokyo, Japan. In Plos One, 2012
Genetic factors regarded as putative risk factors were RA-susceptible polymorphisms identified by the Japanese GWAS meta-analysis, including HLA-DRB1 (shared epitope, SE), rs2240340 (PADI4), rs2230926 (TNFAIP3), rs3093024 (CCR6), rs11900673 (B3GNT2), rs2867461 (ANXA3), rs657075 (CSF2), rs12529514 (CD83), rs2233434 (NFKBIE), rs10821944 (ARID5B), rs3781913 (PDE2A-ARAP1), rs2841277 (PLD4) and rs2847297 (PTPN2).
Functional variants in NFKBIE and RTKN2 involved in activation of the NF-κB pathway are associated with rheumatoid arthritis in Japanese.
Yamamoto et al., Yokohama, Japan. In Plos Genet, 2012
Through a genome-wide association study (GWAS) and two replication studies in the Japanese population (7,907 cases and 35,362 controls), we identified two gene loci associated with rheumatoid arthritis susceptibility (NFKBIE at 6p21.1, rs2233434, odds ratio (OR) = 1.20,
Meta-analysis identifies nine new loci associated with rheumatoid arthritis in the Japanese population.
Yamamoto et al., Yokohama, Japan. In Nat Genet, 2012
Our study identified nine loci newly associated with rheumatoid arthritis at a threshold of P < 5.0 × 10(-8), including B3GNT2, ANXA3, CSF2, CD83, NFKBIE, ARID5B, PDE2A-ARAP1, PLD4 and PTPN2.
Inhibitor of kappa B epsilon (IκBε) is a non-redundant regulator of c-Rel-dependent gene expression in murine T and B cells.
Cope et al., London, United Kingdom. In Plos One, 2010
The data imply that regulation of these c-Rel-dependent lymphoid responses is a non-redundant function of IkappaBepsilon.
Gene expression levels in normal human lymphoblasts with variable sensitivities to arsenite: identification of GGT1 and NFKBIE expression levels as possible biomarkers of susceptibility.
Rossman et al., New York City, United States. In Toxicol Appl Pharmacol, 2008
Expression levels of GGT1 and possibly NFKBIE might be useful as biomarkers of genetic susceptibility to arsenite.
IkappaB genetic polymorphisms and invasive pneumococcal disease.
Hill et al., Oxford, United Kingdom. In Am J Respir Crit Care Med, 2007
An NFKBIE SNP associated with susceptibility to pneumococcal disease but not pneumococcal empyema.
A homeostatic model of IkappaB metabolism to control constitutive NF-kappaB activity.
Hoffmann et al., Los Angeles, United States. In Mol Syst Biol, 2006
In vivo degradation rate constants were measured for NF-kappaB-bound & -unbound IkappaB. Models suggest differential degradation rates of free & bound IkappaB may be a new cross-regulation mechanism imparting functional robustness to the signaling module.
Protein phosphatase 6 subunit with conserved Sit4-associated protein domain targets IkappaBepsilon.
Brautigan et al., Charlottesville, United States. In J Biol Chem, 2006
Protein phosphatase 6 subunit with conserved Sit4-associated protein domain targets IkappaBepsilon
Distinct roles of IkappaB proteins in regulating constitutive NF-kappaB activity.
Verma et al., Los Angeles, United States. In Nat Cell Biol, 2005
We show that in cells depleted of IkappaBalpha, IkappaBbeta and IkappaBepsilon proteins, a small fraction of p65 binds DNA and leads to constitutive activation of NF-kappaB target genes, even without stimulation, whereas most of the p65 remains cytoplasmic.
[Human pathologies associated with NF-kappaB defects].
Israël et al., Paris, France. In J Soc Biol, 2003
Three of these inhibitory molecules have been described: IkappaBalpha, IkappaBbeta and IkappaBepsilon.
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