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anti-Human IKBKG Antibodies:
anti-Mouse (Murine) IKBKG Antibodies:
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Human Monoclonal IKBKG Primary Antibody for SimWes, WB - ABIN252501
Wunderlich, Luedde, Singer, Schmidt-Supprian, Baumgartl, Schirmacher, Pasparakis, Brüning: Hepatic NF-kappa B essential modulator deficiency prevents obesity-induced insulin resistance but synergizes with high-fat feeding in tumorigenesis. in Proceedings of the National Academy of Sciences of the United States of America 2008
Show all 7 Pubmed References
Human Monoclonal IKBKG Primary Antibody for ICS - ABIN1177069
Carter, Pennington, Ungurait, Ballard: In vivo identification of inducible phosphoacceptors in the IKKgamma/NEMO subunit of human IkappaB kinase. in The Journal of biological chemistry 2003
Show all 6 Pubmed References
Human Monoclonal IKBKG Primary Antibody for ELISA - ABIN4324315
Han, Karabiyikoglu, Kelly, Sobel, Yenari: Mild hypothermia inhibits nuclear factor-kappaB translocation in experimental stroke. in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 2003
Show all 5 Pubmed References
Human Monoclonal IKBKG Primary Antibody for FACS, WB - ABIN252492
Harhaj, Sun: IKKgamma serves as a docking subunit of the IkappaB kinase (IKK) and mediates interaction of IKK with the human T-cell leukemia virus Tax protein. in The Journal of biological chemistry 1999
Show all 5 Pubmed References
Human Monoclonal IKBKG Primary Antibody for ELISA, WB - ABIN533000
Fusco, DUrso, Miano, Ursini: The LCR at the IKBKG locus is prone to recombine. in American journal of human genetics 2010
Show all 3 Pubmed References
Human Polyclonal IKBKG Primary Antibody for ICC, ELISA - ABIN1002508
Li, Kang, Friedman, Tarassishin, Ye, Kovalenko, Wallach, Horwitz: Identification of a cell protein (FIP-3) as a modulator of NF-kappaB activity and as a target of an adenovirus inhibitor of tumor necrosis factor alpha-induced apoptosis. in Proceedings of the National Academy of Sciences of the United States of America 1999
Show all 4 Pubmed References
Human Polyclonal IKBKG Primary Antibody for IHC, WB - ABIN6672282
Guo, Hu, Chen, Li, Ye, Cheng, Zhang, He: iTRAQ-based comparative proteomic analysis of Vero cells infected with virulent and CV777 vaccine strain-like strains of porcine epidemic diarrhea virus. in Journal of proteomics 2016
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Mouse (Murine) Polyclonal IKBKG Primary Antibody for IHC, WB - ABIN3021151
Zhu, Fang, Wang, Yang, Chen, Ye, Foda, Xiao: Porcine deltacoronavirus nsp5 inhibits interferon-β production through the cleavage of NEMO. in Virology 2017
Show all 2 Pubmed References
Human Monoclonal IKBKG Primary Antibody for WB - ABIN6664264
Wang, Fang, Wei, Zhang, Luo, Chen, Li, Xiao: Hepatitis A virus 3C protease cleaves NEMO to impair induction of beta interferon. in Journal of virology 2014
Ectodermal dysplasia with immunodeficiency caused by a branch-point mutation in IKBKG/NEMO.
This was the first study suggesting the relevant role of NEMO/IKKgamma protein, and highlights the prognostic significance with outcome in uveal melanoma patients
Computational analysis identified two miR-107 binding sites in the 3'UTR of IKBKG suggesting that IKBKG expression is regulated by miR-107.
Human IKKgamma does not interact with mammalian Atg8-family proteins.
Data suggest the angiopoietin-like 8 (ANGPTL8)/p62-IKKgamma axis as a negative feedback loop that regulates NF-kappaB activation, and extends the role of selective autophagy in fine-tuned inflammatory responses.
this study demonstrates immunodeficiency in two female patients with Incontinentia Pigmenti with heterozygous NEMO mutation diagnosed by lipopolysaccharide unresponsiveness
GSK-3beta is critically important for ordered NF-kappaB signalling through modulation of NEMO phosphorylation.
HOTAIR operates the action of IKKalpha, IKKbeta, IKKgamma in liver cancer stem cells
the present study found that loss of the NEMO-SHARPIN interaction impaired recruitment of truncated NEMO forms into punctuate structures that are transiently formed on cell stimulation and thus led to a defect in linear ubiquitination
NEMO was critically involved in the cGAS-STING pathway.
Results show that NEMO's expression is regulated by ASAP3 which it interacts directly with it reducing its poly-ubiquitinylation.
E+P treatment of breast cancer cells increased ER binding to the NEMO promoter, thereby increasing NEMO expression.
Hematopoietic stem cell transplantation can cure most clinical features of patients with a variety of IKBKG mutations.
Authors show that NEMO stabilizes HIFalpha via direct interaction and independently of NF-kappaB signaling in vitro. NEMO prolongs tumor cell survival via regulation of apoptosis and activation of epithelial-to-mesenchymal transition, facilitating tumor metastasis.
The results demonstrate the the first example of father-to-daughter transmission of IP in which a pathogenic mutation in IKBKG has been demonstrated
Molluscum contagiosum virus MC005 inhibited NF-kappaB proximal to the IkappaB kinase (IKK) complex, and unbiased affinity purification revealed that MC005 interacts with the IKK subunit NEMO (NF-kappaB essential modulator).
These data suggest that molluscum contagiosum virus MC159 competitively binds to NEMO to prevent cIAP1-induced NEMO polyubiquitination.
High IKBKG expression is associated with multiple myeloma.
Our findings shed light on the nature of the interaction between NEMO and poly-ubiquitin, suggesting that NEMO is differentially regulated by poly-ubiquitin chain length and that this regulation occurs via a modulation of the available equilibrium of conformational states, rather than gross structural change
FADD, as well as NEMO, is a substrate for LUBAC ubiquitin ligase (E3) complex, composed of the HOIP, HOIL-1L, and SHARPIN subunits.
High NEMO expression is associated with hepatitis and hepatocarcinogenesis.
NEMO deficiency hampered activation of IKK complex in osteoclast precursors, causing arrest of osteoclastogenesis and apoptosis. Interestingly, inhibiting apoptosis by genetic ablation of TNFr1 significantly increased cell survival, but failed to rescue osteoclastogenesis or reverse osteopetrosis.
This study provides evidence for a protective function of canonical IKK/NF-kappaB signalling in the arenchymal compartment during pancreatitis. In the absence of the regulatory IKK subunit NEMO, a combination of a fibrogenic gene signature, enhanced acinar-ductal metaplasia and a lack of regeneration contribute to the exacerbation of pancreatitis.
robust caspase activation in NEMO-deficient cells is concomitant with RIPK3 recruitment to the apoptosis-mediating complex.
lymphocyte-specific deletion of IKK2 or NEMO aggravated kidney injury after ischemia-reperfusion injury, and, in both conditions, the percentage of Th17 cells was increased.
Whereas Parkin has been reported to positively regulate the expression of OPA1 through NEMO, herein we found that PARK2 overexpression did not modify the expression of OPA1.
prevents colon inflammation by NF-kappaB-independent functions
Thyrocyte-specific NEMO knock-out mice gradually develop hypothyroidism after birth, which leads to reduced body weight and shortened life span.
SENP1 deletion in adipocytes causes Type 1 diabetes mellitus via enhanced SUMOylation of NEMO, leading to increased NF-kappaB activity, cytokine production and pancreatic inflammation.
Crucial functions of inflammatory TAK1-NEMO signaling in protecting the brain endothelium and maintaining normal brain function.
Data show that NEMO protein prevents hepatocarcinogenesis by inhibiting receptor (TNFRSF)-interacting serine-threonine kinase 1 (RIPK1) kinase activity-driven hepatocyte apoptosis.
Data show that the in utero death of NF-NF-kappaB essential modulator (NEMO) and cylindromatosis protein double mutant mice is mediated by TNF receptor 1 (TNFR1) signaling and can be rescued by TNFR1 deficiency.
signaling through NEMO might not only be involved in the production of NF-kappaB proinflammatory chemokines but also regulates podocyte dynamics independently of NF-kappaB
The stability of the NEMO coiled coil is maintained by strong interhelix interactions in the region centered on residue 54.
NEMO deficiency results in apoptosis, the development of liver fibrosis and hepatocellular carcinoma, all of which are substantially alleviated by allogeneic hepatocyte transplantation.
Mass spectrometric analysis demonstrated that WA covalently modifies NEMO on a cysteine residue within the C-terminal zinc finger (ZF) domain. Point mutations to the ZF can reverse the WA-induced Lys-48-polyubiquitin binding phenotype
Authors propose a model in murine cytomegalovirus virion-associated protein M45 delivered by viral particles activates NF-kappaB, presumably involving an interaction with RIP1 and NEMO.
NEMO ubiquitination is required for optimal innate immune signaling responses. These findings suggest that NEMO ubiquitination is crucial for NF-kappaB activity in response to innate immune agonists.
Drosophila Kenny is a selective autophagy receptor that mediates the degradation of the IkappaB kinase complex. Selective autophagic degradation of the IkappaB kinase complex prevents constitutive activation of the immune deficiency pathway in response to commensal microbiota. We show that autophagy-deficient flies have a systemic innate immune response that promotes a hyperplasia phenotype in the midgut.
Porcine deltacoronavirus nsp5, the 3C-like protease, inhibits interferon-beta production through the cleavage of NEMO.
Nsp4 interfered with the NF-kappaB signaling pathway through the cleavage of IKBKG at the E349-S350 site, leading to the downregulation of IFN-beta production.
Foot-and-mouth disease virus 3C protease cleaves NEMO to impair innate immune signaling.
This gene encodes the regulatory subunit of the inhibitor of kappaB kinase (IKK) complex, which activates NF-kappaB resulting in activation of genes involved in inflammation, immunity, cell survival, and other pathways. Mutations in this gene result in incontinentia pigmenti, hypohidrotic ectodermal dysplasia, and several other types of immunodeficiencies. Multiple transcript variants encoding different isoforms have been found for this gene. A pseudogene highly similar to this locus is located in an adjacent region of the X chromosome.
I-kappa-B kinase subunit gamma
, IkB kinase gamma subunit
, NF-kappa-B essential modifier
, NF-kappa-B essential modulator
, NFkappaB essential modulator
, ikB kinase subunit gamma
, ikB kinase-associated protein 1
, incontinentia pigmenti
, inhibitor of nuclear factor kappa-B kinase subunit gamma
, inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase gamma
, I-kappa-B kinase gamma
, NF-kappa B essential modulator
, inhibitor of kappaB kinase gamma
, inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase gamma, isoform 1
, inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase gamma, isoform 2
, NF-kappa-B essential modulator-like