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Conserved helix-loop-helix ubiquitous kinase

I-kappa B Kinase, IKKalpha
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: NF-kappaB, IKKbeta, IkappaBalpha, p65, V1a
Papers using I-kappa B Kinase antibodies
Involvement of reactive oxygen species in toll-like receptor 4-dependent activation of NFκB
Chang Alice Y. W., In PLoS ONE, 2003
... Bay 11-7082, a selective IkappaB kinase (IKK) inhibitor was obtained from Cayman Chemical (Ann Arbor, MI) ...
Papers on I-kappa B Kinase
Silencing of the cell cycle checkpoint gene 14-3-3σ in basal cell carcinomas correlates with reduced expression of IKK-α.
Herzinger et al., München, Germany. In J Eur Acad Dermatol Venereol, Aug 2014
IkappaB kinase α (IKK-α), one of the two catalytic subunits of the IKK complex involved in NF-kappaB-activation, also functions as a modulator of epidermal development and differentiation.
Tumor suppressor PDCD4 inhibits NF-κB-dependent transcription in human glioblastoma cells by direct interaction with p65.
Colburn et al., Frederick, United States. In Carcinogenesis, Jul 2014
PDCD4 does not inhibit pathways upstream of NF-κB including the activation of IKKα and IKKβ kinases or degradation of IκBα, events needed for nuclear transport of p65 and p50.
Spatial control of bone formation using a porous polymer scaffold co-delivering anabolic rhBMP-2 and anti-resorptive agents.
Schindeler et al., Westmead, Australia. In Eur Cell Mater, Dec 2013
Scaffolds were encapsulated with anabolic rhBMP-2 (20 µg) ± anti-resorptive agents: zoledronic acid (5 µg ZA), ZA pre-adsorbed onto hydroxyapatite microparticles, (5 µg ZA/2% HA) or IkappaB kinase (IKK) inhibitor (10 µg PS-1145).
A20-mediated negative regulation of canonical NF-κB signaling pathway.
Shembade et al., Miami, United States. In Immunol Res, Dec 2013
All known NF-κB activators converge on the IkappaB kinase (IKK) complex to activate the canonical and non-canonical NF-κB pathways.
Acetylpuerarin reduces inflammation and improves memory function in a rat model of Alzheimer's disease induced by Abeta1-42.
Zhang et al., Jinan, China. In Pharmazie, Nov 2013
Immunohistochemistry was used to assess expression levels of ionized calcium-binding adaptor molecule (Ibal), protein kinase C delta (PKCdelta), IkappaB kinase beta (IKKbeta), and inducible nitric oxide synthase (iNOS) in hippocampus.
Resveratrol inhibits NF-kB signaling through suppression of p65 and IkappaB kinase activities.
Yang et al., Guangzhou, China. In Pharmazie, Aug 2013
Further investigation revealed that resveratrol blocked the ubiquitination of NEMO and inhibited IkappaB kinase(beta)-mediated NF-kappaB activation.
HTLV-1 tax-induced rapid senescence is driven by the transcriptional activity of NF-κB and depends on chronically activated IKKα and p65/RelA.
Giam et al., Bethesda, United States. In J Virol, 2012
HTLV-1 tax-induced rapid senescence is driven by the transcriptional activity of NF-kappaB and depends on chronically activated IKKalpha and RelA.
A role for the NF-κB pathway in cell protection from complement-dependent cytotoxicity.
Fishelson et al., Tel Aviv-Yafo, Israel. In J Immunol, 2012
Embryonic fibroblasts lacking either the p65 subunit of NF-kappaB or the IkappaB kinase alpha or IkappaB beta subunits of the NF-kappaB activator complex are more sensitive to complement-dependent cytotoxicity.
IκB kinase α phosphorylation of TRAF4 downregulates innate immune signaling.
Abbott et al., Cleveland, United States. In Mol Cell Biol, 2012
Like IKKalpha, TRAF4 is atypical within its family because it is the only TRAF family member to negatively regulate innate immune signaling. IKKalpha's phosphorylation of serine-426 on TRAF4 was required for this negative regulation.
The microRNA miR-23b suppresses IL-17-associated autoimmune inflammation by targeting TAB2, TAB3 and IKK-α.
Qian et al., Shanghai, China. In Nat Med, 2012
MiR-23b suppresses IL-17-, tumor necrosis factor alpha (TNF-alpha)- or IL-1beta-induced NF-kappaB activation and inflammatory cytokine expression by targeting TAB2, TAB3 and IKK-alpha.
IKKα-mediated signaling circuitry regulates early B lymphopoiesis during hematopoiesis.
Hu et al., Frederick, United States. In Blood, 2012
This study found defective bone marrow B-cell development and increased myeloid-erythroid lineages in kinase-dead IKK alpha (KA/KA) knock-in mice.
The role of TNF and Fas dependent signaling in animal models of inflammatory liver injury and liver cancer.
Trautwein et al., Aachen, Germany. In Eur J Cell Biol, 2012
By using conditional knockout technology in mice we genetically dissected the I-kappa B kinase (IKK) complex consisting of IKK1/IKKα, IKK2/IKKβ and IKKγ/NEMO.
[Research progress of the biological characteristics of IkappaB kinase and its inhibitors].
Wu et al., Chaohu, China. In Yao Xue Xue Bao, 2011
IkappaB kinase (IKK) is the key of this pathway, and it owns a special structure which consists of catalytic subunit and regulatory subunit.
MicroRNAs modulate the noncanonical transcription factor NF-kappaB pathway by regulating expression of the kinase IKKalpha during macrophage differentiation.
Liu et al., Bethesda, United States. In Nat Immunol, 2010
during human monocyte-macrophage differentiation, expression of the microRNAs miR-223, miR-15a and miR-16 decreased considerably, which led to higher expression of the serine-threonine kinase IKKalpha in macrophages
Sphingosine-1-phosphate is a missing cofactor for the E3 ubiquitin ligase TRAF2.
Spiegel et al., Richmond, United States. In Nature, 2010
Genetic evidence indicates that TRAF2 is necessary for the polyubiquitination of receptor interacting protein 1 (RIP1) that then serves as a platform for recruitment and stimulation of IkappaB kinase, leading to activation of the transcription factor NF-kappaB.
Oncogenic activation of NF-kappaB.
Staudt, Bethesda, United States. In Cold Spring Harb Perspect Biol, 2010
Many genetic aberrations in lymphomas alter CARD11, MALT1, or BCL10, which constitute a signaling complex that is intermediate between the B-cell receptor and IkappaB kinase.
NLRC5 negatively regulates the NF-kappaB and type I interferon signaling pathways.
Wang et al., Houston, United States. In Cell, 2010
NLRC5 inhibited NF-kappaB-dependent responses by interacting with IKKalpha and IKKbeta and blocking their phosphorylation.
NF-kappaB signaling: a tale of two pathways in skeletal myogenesis.
Guttridge et al., Columbus, United States. In Physiol Rev, 2010
Activation of NF-kappaB is controlled by an IkappaB kinase (IKK) complex that can direct either canonical (classical) NF-kappaB signaling by degrading the IkappaB inhibitor and releasing p65/p50 dimers to the nucleus, or causes p100 processing and nuclear translocation of RelB/p52 via a noncanonical (alternative) pathway.
B-cell-derived lymphotoxin promotes castration-resistant prostate cancer.
Karin et al., San Diego, United States. In Nature, 2010
The inflammation-responsive IkappaB kinase (IKK)-beta and its target NF-kappaB have important tumour-promoting functions within malignant cells and inflammatory cells.
The IKK complex, a central regulator of NF-kappaB activation.
Israël, Paris, France. In Cold Spring Harb Perspect Biol, 2010
It is essentially made of two kinases (IKKalpha and IKKbeta) and a regulatory subunit, NEMO/IKKgamma.
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