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miR379 inhibits cell proliferation and epithelialmesenchymal transition by targeting CHUK through the NFkappaB pathway in nonsmall cell lung cancer.
Data suggest a linkage between notch receptor 1 (NOTCH1), IKK-alpha protein (IKKalpha), and NF-kappa B (NF-kappaB) pathway activation in maintaining the CD133(+) stem cutaneous squamous cell carcinoma (cSCC) phenotypes.
mRNA expression of individual inhibitory kappaB kinases and SIKE are associated with unique prognostic significance and may act as valuable prognostic biomarkers and potential targets for future therapeutic interventions in gastric cancer.
Data indicate that DEAD-box helicase 3 (DDX3) directly interacts with IkappaB kinase alpha (IKKalpha) and enhances its autophosphorylation and -activation.
A core element of NF-kappaB activation is the IKK complex built from two catalytic subunits, IKKa and IKKb kinases, and a regulatory subunit, NF-kappaB essential modulator (NEMO)/IKKc. (Review)
Depletion of human IKK1, IKK2 or IKK1/2 leads to strongly impaired NF-kappaB activation. Only IKK1/2 double-deficient cells are sensitized to TNF-alpha induced cell death. Cell death is mediated independently on NF-kappaB via RIPK1.
AMBRA1 regulates mitophagy through a novel pathway, in which HUWE1 and IKKalpha are key factors, shedding new lights on the regulation of mitochondrial quality control and homoeostasis in mammalian cells.
evidence that DCNL5 may be involved in innate immunity, as it is a direct substrate of the kinase IKKalpha during immune signalling.
cFLIP appears to bind to IKKalpha to prevent IKKalpha from phosphorylating and activating IRF7.
functions as a suppressor of lung adenocarcinoma; deletion up-regulates NOX2 and down-regulates NRF2, leading to ROS accumulation and blockade of cell senescence induction
HOTAIR operates the action of IKKalpha, IKKbeta, IKKgamma in liver cancer stem cells
Results indicate the involvement of IKK and NF-kappaB signaling in the maintenance of glioblastoma stem cell.
Loss-of-function of LINC00473 in vivo effectively promoted the regression of Wilms tumour via miR-195/IKKalpha-mediated growth inhibition.
Study results provide new insights into the molecular mechanisms of maspin suppression in response to HBx, and revealed nuclear IKKalpha as a prognostic biomarker and a potential therapeutic target to improve the clinical outcome of HBV-associated HCC patients.
Data show that IKKalpha directly bind to the promoters of LGR5, in turn, upregulating LGR5 expression through activation of STAT3 signaling pathway during cancer progression.
single-particle cryoelectron microscopy (cryo-EM) and X-ray crystal structures of human IKK1 in dimeric ( approximately 150 kDa) and hexameric ( approximately 450 kDa) forms, are reported.
results suggest that changes in the relative concentrations of RelB, NIK:IKK1, and p100 during noncanonical signaling modulate this transitional complex and are critical for maintaining the fine balance between the processing and protection of p100.
IKKalpha-dependent phosphorylation of S376 stimulated whereas IKKalpha-independent phosphorylation of S484 inhibited RORgammat function in Th17 differentiation.
Akt2, Erk2, and IKK1/2 phosphorylate Bcl3, converting Bcl3 into a transcriptional coregulator by facilitating its recruitment to DNA.
IKKalpha promotes migration through dynamic interactions with the EGF promoter depending on the redox state within cells.
The data show that IKKa and IKKb regulate unique genes in pulmonary endothelial cells, resulting in differential effects on lung angiogenesis.
our data reveals that IKKa is a novel mediator protecting against the development of myocardial I/R injury via negative regulation of macrophage polarization to M1 phenotype.
Data suggest a direct link between microtubule-associated protein 1-light chain 3 (LC3)-associated phagocytosis (LAP) formation and IKK alpha (IKKalpha) recruitment downstream of -like receptor 9 (TLR9) activation that is necessary to facilitate type I IFN production.
Data show that IkappaB kinase (IKK) controlled thymocyte survival by repressing cell-death-inducing activity of the serine/threonine kinase RIPK1 (RIPK1).
IKKalpha knockout disrupts cell differentiation and migration of marginal zone and follicular B cells.
Deficiency of IKKalpha prevents adenoma formation, with adenomas lacking IKKalpha showing reduced proliferation. In contrast, IKKalpha status did not affect normal intestinal function. The same divergent phenotype was found in the organoid-spheroid model.
Pathological activation of hepatic IKK alpha likely blocks hepatocyte replication, contributing to liver disease progression.
By modulating the translation of IkappaBalpha via the Mnk2-eIF4E pathway, Brd4 provides an additional layer of control for NF-kappaB-dependent inflammatory gene expression and inflammatory response.
UVB-irradiated or aged mice skin revealed that mTORC2 activity was significantly upregulated which in turn increased Akt activation and Akt-dependent IkappaB kinase alpha (IKKalpha) phosphorylation, and The increased mTORC2 signaling pathway during skin aging were associated to NF-kappaB activation.
Filiform papillae thus develop through distinct molecular mechanisms between the regions of tongue dorsum in the medio-lateral axis, with some filiform papillae developing under the control of Ikkalpha and Irf6.
IKKalpha as a central mediator sensing both cytokine and microbial stimulation to suppress endoplasmic reticulum stress, thereby assuring antiinflammatory function during acute intestinal inflammation.
The kinase IKKalpha inhibits activation of the transcription factor NF-kappaB by phosphorylating the regulatory molecule TAX1BP1.
Data indicate that the inflammation and proliferation-related functions of I kappa B kinase (IKKbeta) can be uncoupled by quinoxaline urea analog 13-197.
Hematopoietic IKKalpha deficiency in mouse suppresses Akt signaling, compromising monocyte/macrophage survival and this decreases early atherosclerosis.
Anatomy of a negative feedback loop: the case of IkappaBalpha.
Epithelial-intrinsic IKK-alpha expression regulates group 3 innate lymphoid cell responses and antibacterial immunity.
These findings reveal a molecular mechanism regulating migration and invasion of epithelial cells and establish a key direct link between IKKbeta and cell motility controlled by Rap-integrin signaling.
poky/chuk/ikk1 is required for differentiation of the zebrafish embryonic epidermis
Ikk1 negatively regulates NF-kappaB by sequestering NEMO from active IKK complexes, indicating that IKK1 can function as a repressor of NF-kappaB.
This gene encodes a member of the serine/threonine protein kinase family. The encoded protein, a component of a cytokine-activated protein complex that is an inhibitor of the essential transcription factor NF-kappa-B complex, phosphorylates sites that trigger the degradation of the inhibitor via the ubiquination pathway, thereby activating the transcription factor.
, i kappa-B kinase alpha
, inhibitor of nuclear factor kappa-B kinase subunit alpha
, nuclear factor NF-kappa-B inhibitor kinase alpha
, SPFH domain-containing protein 1
, conserved helix-loop-helix ubiquitous kinase
, I-kappa-B kinase 1
, I-kappa-B kinase-alpha
, IKK-a kinase
, IkB kinase alpha subunit
, Nuclear factor NFkappaB inhibitor kinase alpha
, transcription factor 16
, I kappa B kinase 1
, I-kappa-B kinase alpha
, IKK alpha
, IkappaB kinase alpha
, ikappaB kinase
, IkB kinase-a