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crystal structure of IKKbeta in complex with an inhibitor, at a resolution of 3.6 A
High IKBKB expression is associated with prostate cancer.
Akt2 (show AKT2 ELISA Kits), Erk2 (show MAPK1 ELISA Kits), and IKK1 (show CHUK ELISA Kits)/2 phosphorylate Bcl3 (show BCL3 ELISA Kits), converting Bcl3 (show BCL3 ELISA Kits) into a transcriptional coregulator by facilitating its recruitment to DNA.
Rare variants in IKBKB are associated with decreased waist-to-hip ratio in European-Americans.
pVHL (show VHL ELISA Kits) mediates K63-linked ubiquitination of IKKbeta, which plays a role in the regulation of IKK (show CHUK ELISA Kits)/NF-kappaB (show NFKB1 ELISA Kits) signalling.
N-acetyl-seryl-aspartyl-lysyl-proline inhibition of TNF-alpha (show TNF ELISA Kits) activation of canonical, i.e., IKK-beta-dependent, NF-kappaB (show NFKB1 ELISA Kits) pathway and subsequent decrease in ICAM-1 (show ICAM1 ELISA Kits) expression is achieved via inhibition of IKK-beta.
our results demonstrate that miR (show MLXIP ELISA Kits)-200b, a transcriptional target of NF-kappaB (show NFKB1 ELISA Kits), suppresses breast cancer cell growth and migration, and NF-kappaB (show NFKB1 ELISA Kits) activation, through downregulation of IKBKB, indicating that miR (show MLXIP ELISA Kits)-200b has potential as a therapeutic target in breast cancer patients.
The present research concluded that aspirin suppressed prostate cancer cell invasion by reducing MMP-9 (show MMP9 ELISA Kits) activity and uPA (show PRAP1 ELISA Kits) expression through decreasing of IKK-beta-mediated NF-kappaB (show NFKB1 ELISA Kits) activation, indicating that the ability of aspirin to inhibit cell invasion might be useful in the chemoprevention of metastatic prostate cancer.
miR (show MLXIP ELISA Kits)-429 is involved in regulation of the NF-kappaB (show NFKB1 ELISA Kits) pathway by targeting IKKbeta and functions as a tumor suppressor in cervical carcinogenesis.
TLR signaling led to lower expression of LRRC14 (show LRRC14 ELISA Kits).
results uncover a previously unidentified role of IKKbeta in regulating glycolysis, sensing low-glutamine-induced metabolic stress, and promoting cellular adaptation to nutrient availability.
Staphylococcus aureus infection inhibits nuclear factor kappa B activation mediated by prolactin (show PRL ELISA Kits) in bovine mammary epithelial cells.
Elevated levels of common free fatty acids found in human serum activate IKKbeta in bovine endothelial cells leading to reduced nitric oxide, and may serve to link pathways involved in inflammation and endothelial dysfunction.
High glucose treatment also activated IKKbeta, and pretreatment with aspirin, a pharmacological inhibitor of IKKbeta, prevented both glucose-induced IKKbeta activation and the effect of high glucose to impair insulin (show INS ELISA Kits)-mediated NO production.
High glucose-induced IKK (show CHUK ELISA Kits)-Hsp-90 (show HSP90 ELISA Kits) interaction contributes to endothelial dysfunction.
Myeloid IKKbeta deficiency prevents Western diet-induced obesity and visceral adiposity in females but not in males, and attenuates hyperglycemia, global insulin (show INS ELISA Kits) 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.
lymphocyte-specific deletion of IKK2 or NEMO (show IKBKG ELISA Kits) aggravated kidney injury after ischemia-reperfusion injury, and, in both conditions, the percentage of Th17 cells was increased.
data clearly demonstrate that KLHL21 (show KLHL21 ELISA Kits) negatively regulates TNFalpha (show TNF ELISA Kits)-activated NF-kappaB (show NFKB1 ELISA Kits) signaling via targeting IKKbeta, providing new insight into the mechanisms underlying NF-kappaB (show NFKB1 ELISA Kits) regulation in cells.
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 (show INS ELISA Kits) sensitivity and consequently in glucose homeostasis.
Mutation of cysteine 46 in IKK-beta increases inflammatory responses.
TAK1 (show NR2C2 ELISA Kits) and IKK2 are novel mediators of SCF (show KITLG ELISA Kits)-induced signaling and potential targets for c-Kit (show KIT ELISA Kits)-driven diseases.
MyD88s is positively regulated by IKKbeta and CREB (show CREB1 ELISA Kits) and negatively regulated by ERK1/2 (show MAPK1/3 ELISA Kits) signaling pathways.
these results highlight an unexpected tumor suppressive function of IKKbeta/NF-kappaB (show NFKB1 ELISA Kits) in cancer-associated fibroblasts.
These results reveal a hitherto unknown role of mesenchymal IKKbeta in driving inflammation and enabling carcinogenesis in the intestine.
results provide evidence for a previously unrecognized role of IKKbeta in the regulation of the growth plate that is mediated through stimulation-independent downregulation of MCP-5 (show CMA1 ELISA Kits) in the perichondrium.
The protein encoded by this gene phosphorylates the inhibitor in the inhibitor/NF-kappa-B complex, causing dissociation of the inhibitor and activation of NF-kappa-B. The encoded protein itself is found in a complex of proteins. Several transcript variants, some protein-coding and some not, have been found for this gene.
inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase beta
, inhibitor of nuclear factor kappa-B kinase subunit beta
, inhibitor of nuclear factor kappa-B kinase subunit beta-like
, IKK-like protein
, LPS-responsive kinase
, cactus kinase
, deficient 5
, immune response
, lipopolysaccharide activated kinase
, mmune response deficient 5
, I-kappa-B kinase 2
, I-kappa-B-kinase beta
, nuclear factor NF-kappa-B inhibitor kinase beta
, inhibitor of kappaB kinase beta
, inhibitor of nuclear factor kappa B kinase beta subunit
, inhibitor of kappa light chain gene enhancer in B cells, kinase beta