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

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

IkappaB-zeta, MAIL, NFKBIZ, INAP
This gene is a member of the ankyrin-repeat family and is induced by lipopolysaccharide (LPS). The C-terminal portion of the encoded product which contains the ankyrin repeats, shares high sequence similarity with the I kappa B family of proteins. The latter are known to play a role in inflammatory responses to LPS by their interaction with NF-B proteins through ankyrin-repeat domains. Studies in mouse indicate that this gene product is one of the nuclear I kappa B proteins and an activator of IL-6 production. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2008] (from NCBI)
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Top mentioned proteins: NF-kappaB, IL-1beta, Interleukin-6, IL-17, CAN
Papers on IkappaB-zeta
Targetable genetic features of primary testicular and primary central nervous system lymphomas.
Shipp et al., Boston, United States. In Blood, Jan 2016
PCNSLs and PTLs also utilize multiple genetic mechanisms to target key genes and pathways and exhibit near-uniform oncogenic Toll-like receptor signaling due to MYD88 mutation and/or NFKBIZ amplification, frequent concurrent B-cell receptor pathway activation and deregulation of BCL6.
Genetic landscapes of relapsed and refractory diffuse large B cell lymphomas.
Johnson et al., Vancouver, Canada. In Clin Cancer Res, Jan 2016
RESULTS: Based on the a higher frequency at relapse and evidence for clonal selection, TP53, FOXO1, MLL3, CCND3, NFKBIZ and STAT6 emerged as top candidate genes implicated in therapeutic resistance.
A mix of S and ΔS variants of STAT3 enable survival of activated B-cell-like diffuse large B-cell lymphoma cells in culture.
Rui et al., Madison, United States. In Oncogenesis, Dec 2015
Rescue correlated with expression of STAT3-sensitive genes NFKBIA and NFKBIZ.
MCPIP1 Endoribonuclease Activity Negatively Regulates Interleukin-17-Mediated Signaling and Inflammation.
Gaffen et al., Pittsburgh, United States. In Immunity, Oct 2015
However, MCPIP1 strongly inhibited the Lcn2 promoter by regulating the mRNA stability of Nfkbiz, encoding the IκBζ transcription factor.
Nfkbiz regulates the proliferation and differentiation of keratinocytes.
Morimatsu et al., In Jpn J Vet Res, Aug 2015
Nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) inhibitor zeta (Nfkbiz) is a nuclear inhibitor of NF-κB (IκB) protein that is also termed as molecule possessing ankyrin repeats induced by lipopolysaccharide, interleukin-1-inducible nuclear ankyrin repeat protein, or IκBζ.
Enhanced meta-analysis and replication studies identify five new psoriasis susceptibility loci.
Elder et al., Ann Arbor, United States. In Nat Commun, 2014
NFKBIZ (3q12.3)
The role of IFN-γ in regulating Nfkbiz expression in epidermal keratinocytes.
Morimatsu et al., Japan. In Biomed Res, 2014
Nfkbiz is an inhibitor of nuclear factor κB (IκB) protein localized to the nucleus.
Downregulation of IL6 Targeted MiR-376b May Contribute to a Positive IL6 Feedback Loop During Early Liver Regeneration in Mice.
Chen et al., Shanghai, China. In Cell Physiol Biochem, 2014
Further target analysis showed that miR-376b reduced the mRNA and protein expression levels of NF-kappa-B inhibitor zeta (NFKBIZ) and signal transducers and transcription activators 3 (STAT3).
Iκb-ζ plays an important role in the ERK-dependent dysregulation of malaria parasite GPI-induced IL-12 expression.
Gowda et al., United States. In Iubmb Life, 2012
extracellular signal regulated kinases modulate IL-12 expression by regulating IkappaB-zeta-dependent binding of NF-kappaB transcription factors to IL-12b gene promoter
Identification of interleukin-1 receptor-associated kinase 1 as a critical component that induces post-transcriptional activation of IκB-ζ.
Muta et al., Sendai, Japan. In Febs J, 2012
investigation of signaling components that induce activation of post-transcriptional mechanism for IkappaB-zeta induction/activation: Activation of IRAK1 or IRAK4, but not TRAF6, is sufficient.
IκBζ augments IL-12- and IL-18-mediated IFN-γ production in human NK cells.
Wewers et al., Columbus, United States. In Blood, 2011
IkappaBzeta functions as an important regulator of IFN-gamma in human NK cells
Legionella pneumophila-induced IκBζ-dependent expression of interleukin-6 in lung epithelium.
Schmeck et al., Berlin, Germany. In Eur Respir J, 2011
analysis of the sequence of flagellin/TLR5- and type IV-dependent IkappaBzeta expression, recruitment of IkappaBzeta/p50 to the il6 promoter, chromatin remodelling and subsequent IL-6 transcription in L. pneumophila-infected lung epithelial cells
IκBζ is essential for natural killer cell activation in response to IL-12 and IL-18.
Takeuchi et al., Ōsaka, Japan. In Proc Natl Acad Sci U S A, 2010
IkappaBzeta is essential for natural killer cell activation in response to IL-12 and IL-18 and antiviral host defense responses.
Ocular surface inflammation mediated by innate immunity.
Kinoshita et al., Kyoto, Japan. In Eye Contact Lens, 2010
Furthermore, we show that IkappaBzeta KO mice exhibit severe, spontaneous ocular surface inflammation accompanied by the eventual loss of almost all goblet cells and spontaneous perioral inflammation.
Gene signature of the metastatic potential of cutaneous melanoma: too much for too little?
Rásó et al., Budapest, Hungary. In Clin Exp Metastasis, 2010
Four studies attempted to define the prognostic signature of skin melanoma but only one based the study on the primary tumor resulting in heterogenous signatures with a minimal overlap (MCM3 and NFKBIZ).
IkappaBzeta regulates T(H)17 development by cooperating with ROR nuclear receptors.
Takayanagi et al., Tokyo, Japan. In Nature, 2010
In cooperation with RORgammat and RORalpha, IkappaBzeta enhances Il17a expression by binding directly to the regulatory region of the Il17a gene
Innate immunity of the ocular surface.
Kinoshita et al., Kyoto, Japan. In Brain Res Bull, 2010
IkappaBzeta is important for TLR signaling, in mice, its knock-out produced severe, spontaneous ocular surface inflammation, the eventual loss of goblet cells, and spontaneous perioral inflammation, suggesting that dysfunction/abnormality of innate immunity can lead to ocular surface inflammation.
NF-kappaB regulation: the nuclear response.
McManus et al., Dublin, Ireland. In J Cell Mol Med, 2009
A number of novel nuclear regulators of NF-kappaB such as IkappaB-zeta and PDZ and LIM domain 2 (PDLIM2) have now been identified, adding another layer to the mechanics of NF-kappaB regulation.
Role of nuclear IkappaB proteins in the regulation of host immune responses.
Takeda et al., Suita, Japan. In J Infect Chemother, 2008
In this review, the in vivo function of the nuclear IkappaB proteins, Bcl-3, IkappaBzeta, and IkappaBNS in the context of host immune responses and diseases will be discussed.
Regulation of Toll/IL-1-receptor-mediated gene expression by the inducible nuclear protein IkappaBzeta.
Akira et al., Suita, Japan. In Nature, 2004
IkappaBzeta is indispensable for the expression of a subset of genes activated in TLR/IL-1R signalling pathways
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