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K63-linked ubiquitination occurs in other kinases at sites homologous to K147 in IKKbeta, including K578 in BRAF V600E, which serves as an oncogenic driver in melanoma and other cancers.
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IKKepsilon plays a key role in the development of valvular remodeling in an aortic valve stenosis model.
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The results demonstrate that the inhibition of miR-16 renders resistance to paclitaxel in vitro and in vivo by targeting IKBKB via NF-kappa B signaling pathway.
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Hepatic overexpression of N-terminal transactivation domain TAp63 induces liver steatosis through IKKbeta activation and the induction of ER stress.
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Astrocyte IKKbeta deletion following high-fat diet-but not before- reduced glucose intolerance and insulin resistance. Hypothalamic inflammation and astrocytosis were reduced in HFD-fed IKKbeta-AKO mice.
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IKKbeta is involved in membrane fusion, and serves as a critical protein kinase required for initial formation and the regulation of the CARMA1/MALT1/Bcl10/CBM complex in platelets.
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NF-kappaB is the transcription factor in regulating many proinflammatory cytokine genes.
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p55TNFR-IKK2-Ripk3 signalling orchestrates arthritogenic and death responses in synovial fibroblasts
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Pulmonary inflammation due to lung-specific overexpression of IKK2ca was sufficient to increase circulating TNFalpha and IL-6 levels, adipose expression of Tnfalpha and Il-6 mRNA, aortic endothelial dysfunction, and systemic insulin resistance.
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prolonged IKKbeta inhibition decimates circulating Tregs and improves Cytotoxic t lymphocytes responses when commenced after tumor vaccination, indicating that IKKbeta represents a druggable checkpoint.
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Results reveal that IKKbeta activity prevents skin tumor development, and shed light on the complex nature of IKKbeta effects on cancer progression, as IKKbeta can both promote and prevent carcinogenesis depending on the cell type or molecular context.
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IKK2 activation in astrocytes initiates selective non-cell-autonomous neurodegeneration
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Chronic overnutrition and astrocytic IKKbeta/NF-kappaB upregulation similarly impaired astrocytic plasticity, leading to sustained shortening of high-order processes. In physiology, astrocytic IKKbeta/NF-kappaB upregulation resulted in early-onset effects, including glucose intolerance and blood pressure rise, and late-onset effects, including body weight and fat gain.
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Expression of both wild-type and catalytically-inactive Y7F mutant GSTP significantly attenuated LPS- or IKKbeta-induced production of GM-CSF. These studies indicate a complex role for GSTP in modulating NF-kappaB, which may involve S-glutathionylation of IKK proteins, and interaction with NF-kappaB family members.
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Myeloid ikkbeta gene deletion significantly reduced the percentage of CD4(+)/IFN-gamma(+) (Th1) and CD4(+)/IL-17(+) (Th17) cells
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Pharmacological and genetic inhibition of IKKbeta decreased voluntary ethanol consumption, providing initial support for IKKbeta as a potential therapeutic target for alcohol abuse.
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Myeloid IKKbeta deficiency prevents Western diet-induced obesity and visceral adiposity in females but not in males, and attenuates hyperglycemia, global insulin resistance, and non-alcoholic steatohepatitis in both genders. In contrast, all metabolic sequela including non-alcoholic steatohepatitis are aggravated by hepatocyte IKKbeta deficiency (IkbkbDeltahep) in male but not female mice.
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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.
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data clearly demonstrate that KLHL21 negatively regulates TNFalpha-activated NF-kappaB signaling via targeting IKKbeta, providing new insight into the mechanisms underlying NF-kappaB regulation in cells.
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Study used three experimental approaches to enhance the IKKbeta activity in the liver of obese mice and observed increased XBP1s activity, reduced endoplasmic reticulum stress, and a significant improvement in insulin sensitivity and consequently in glucose homeostasis.
