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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 (show NFKB1 Proteins) signalling through modulation of NEMO phosphorylation.
HOTAIR operates the action of IKKalpha (show CHUK Proteins), IKKbeta (show IKBKB Proteins), 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 (show ASAP3 Proteins) 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 (show NFKB1 Proteins) 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
NEMO deficiency hampered activation of IKK (show CHUK Proteins) complex in osteoclast precursors, causing arrest of osteoclastogenesis and apoptosis. Interestingly, inhibiting apoptosis by genetic ablation of TNFr1 (show TNFRSF1A Proteins) significantly increased cell survival, but failed to rescue osteoclastogenesis or reverse osteopetrosis (show CSF1 Proteins).
This study provides evidence for a protective function of canonical IKK (show CHUK Proteins)/NF-kappaB (show NFKB1 Proteins) signalling in the arenchymal compartment during pancreatitis. In the absence of the regulatory IKK (show CHUK Proteins) 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 (show CASP3 Proteins) activation in NEMO-deficient cells is concomitant with RIPK3 (show RIPK3 Proteins) recruitment to the apoptosis-mediating complex.
lymphocyte-specific deletion of IKK2 (show IKBKB Proteins) or NEMO aggravated kidney injury after ischemia-reperfusion injury, and, in both conditions, the percentage of Th17 cells was increased.
Whereas Parkin (show PARK2 Proteins) has been reported to positively regulate the expression of OPA1 through NEMO, herein we found that PARK2 (show PARK2 Proteins) overexpression did not modify the expression of OPA1.
prevents colon inflammation by NF-kappaB (show NFKB1 Proteins)-independent functions
Thyrocyte-specific NEMO knock-out mice gradually develop hypothyroidism after birth, which leads to reduced body weight and shortened life span.
SENP1 (show SENP1 Proteins) deletion in adipocytes causes Type 1 diabetes mellitus via enhanced SUMOylation of NEMO, leading to increased NF-kappaB (show NFKB1 Proteins) activity, cytokine production and pancreatic inflammation.
Porcine deltacoronavirus nsp5 (show SPECC1 Proteins), the 3C-like protease, inhibits interferon-beta (show IFNB1 Proteins) production through the cleavage of NEMO.
Nsp4 interfered with the NF-kappaB (show NFKB1 Proteins) signaling pathway through the cleavage of IKBKG at the E349-S350 site, leading to the downregulation of IFN-beta (show IFNB1 Proteins) 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