Aperçu des produits pour anti-NFKBIZ (NFKBIZ) Anticorps

Mouse (Murine) Nuclear Factor of kappa Light Polypeptide Gene Enhancer in B-Cells Inhibitor, zeta (NFKBIZ) interaction partners

1. PDLIM2, known as the ubiquitin E3 ligase, participates in NQO1-dependent IkappaB-zeta degradation.

2. NFkappaBiz differentially regulates NF-kappaB-mediated responses of tubular cells to inflammatory cytokines in a gene-specific manner, and may be of potential therapeutic interest to limit inflammation in kidney disease.

3. Results suggest that the Nfkbiz gene has a potential regulatory role in the microbiota-skin immunity axis.

4. results uncover an important role for IkappaBzeta in IL-36 signaling and validate IkappaBzeta as an attractive target for psoriasis therapy.

5. electrophilic properties of itaconate and derivatives regulate the IkappaBzeta-ATF3 inflammatory axis; results demonstrate that targeting the DI-IkappaBzeta regulatory axis could be an important new strategy for the treatment of IL-17-IkappaBzeta-mediated autoimmune diseases

6. In cultured macrophages, LPS-induced expression of monocyte chemoattractant protein (MCP)-1 was suppressed by NaN3 through inhibition of STAT1 and IkappaBzeta activities.

7. Data show that I-kappa-B-zeta (IkappaBzeta) regulates macrophage interleukin-10 (IL_10) expression by directly activated the Il-10 promoter.

8. A possible important role of Nfkbiz in modulating the progression of inflammatory diseases in which IFN-gamma and IL-1 are abundant.

9. Nfkbiz-/- keratinocytes were hypoproliferative. In skin from Nfkbiz-/- mice, the expression of the keratinocyte differentiation markers K10 and filaggrin were reduced, although that of K14 was unchanged.

10. These data reveal a previously unappreciated role for IkappaB-zeta in IFN-gamma production in T cells and the immunoregulatory function of T regulatory cells.

11. The pyrimidine-rich IkappaBzeta-responsive site plays an essential role in productive interaction of IkappaBzeta with the p50-DNA complex.

12. IkappaB-zeta regulates TLR-mediated CSR by inducing AID

13. The IkappaB-zeta-Akirin2-BAF60 complex physically links the NF-kappaB and SWI/SNF complexes in innate immune cell activation.

14. The IkappaB-zeta-deficient B cells exhibited impaired proliferation and enhanced up-regulation of CD86 following stimulation of TLR9, but not the BCR, indicating critical roles for IkappaB-zeta in TLR signaling in B cells.

15. IkappaBzeta-deficient mice showed significantly impaired CCL2 secretion.

16. Data indicate that expression of IkappaB-zeta in the lacrimal gands requires STAT3.

17. extracellular signal regulated kinases modulate IL-12 expression by regulating IkappaB-zeta-dependent binding of NF-kappaB transcription factors to IL-12b gene promoter

18. IkappaBzeta is essential for natural killer cell activation in response to IL-12 and IL-18 and antiviral host defense responses.

19. In cooperation with RORgammat and RORalpha, IkappaBzeta enhances Il17a expression by binding directly to the regulatory region of the Il17a gene

20. Bacterial lipopolysaccharide induces mRNA expression of an IkappaB MAIL through toll-like receptor 4.

Human Nuclear Factor of kappa Light Polypeptide Gene Enhancer in B-Cells Inhibitor, zeta (NFKBIZ) interaction partners

1. In conclusion, we present IkappaBzeta as a novel key regulator of IL-17A/ F-driven effects in psoriasis.

2. electrophilic properties of itaconate and derivatives regulate the IkappaBzeta-ATF3 inflammatory axis; results demonstrate that targeting the DI-IkappaBzeta regulatory axis could be an important new strategy for the treatment of IL-17-IkappaBzeta-mediated autoimmune diseases

3. we demonstrate that IkappaBzeta, a transcriptional co-activator, may play an important role in psoriasis and possibly other inflammatory diseases by mediating IL-17F- driven effects.

4. this study shows association of common intragenic NFKBIZ polymorphisms with the risk of developing psoriasis

5. a specific IL-17A-induced gene, NFKBIZ, which encodes IkappaB-zeta, a transcriptional regulator for NF-kappaB, was demonstrated to have a significant role for IL-17A-induced gene expression.

6. In cultured macrophages, LPS-induced expression of monocyte chemoattractant protein (MCP)-1 was suppressed by NaN3 through inhibition of STAT1 and IkappaBzeta activities.

7. IkappaB-zeta regulates human monocyte pro-inflammatory responses induced by Streptococcus pneumoniae.

8. TNF-alpha- and IL-17A mediate synergistic induction of DEFB4 gene expression in human keratinocytes through IkappaBzeta

9. We propose a previously unappreciated role of IkappaBzeta in the inflammatory micromilieu as well as progression in glioma

10. These results indicate that the LPS/IL-1beta-MyD88 axis plays a crucial role for stabilization of IkappaB-zeta mRNA.

11. Interferon-gamma (IFN-gamma) interferes with the IL-1/IKB-zeta axis in beta-glucan-activated dendritic cells and promotes T cell-mediated immune responses with increased release of IFN-gamma and IL-22.

12. NFKBIZ gene knockdown in bronchial epithelial cells suppresses the release of IL-1b-induced IL-6 and GMCSF.

13. IkappaBzeta functions as an important regulator of IFN-gamma in human NK cells

14. NF-kappaB-binding cofactor inhibitor of NF-kappaB-zeta (IkappaB-zeta) is constitutively expressed in HTLV-I-infected T cell lines and ATL cells, and Tax transactivates the IkappaB-zeta gene, mainly through NF-kappaB.

15. our data demonstrate that IkappaB-zeta is essential for nuclear NF-kappaB activity in activated B-cell-like subtype of diffuse large B-cell lymphoma

16. 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.

17. 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

18. conclude that multiple NFKBIZ polymorphisms associate with susceptibility to IPD in humans. The study of multiple populations may aid in fine mapping of associations within extensive regions of strong linkage disequilibrium

19. silencing of IkappaBzeta expression led to a specific decrease in IFNgamma production. Overall, our data suggests that IkappaBzeta positively regulates NFkappaB-mediated IFNgamma production in KG-1 cells

20. These results indicate the existence of another signal essential for I kappa B-zeta induction, which is specifically mediated by the Toll/interleukin-1 receptor (TIR) domain-mediated signaling pathway.