gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

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
Contribution of the interaction between rabies virus P protein and IKKε to the inhibition of type I interferon induction signaling.
Nishizono et al., In J Gen Virol, Jan 2016
On the other hand, the P proteins from the RABV street strains 1088 and HCM-9, but not from fixed strains Nishigahara (Ni) and CVS-11 and other lyssaviruses tested, significantly inhibited I-kappa B kinase ε (IKKε)-inducible IRF-3-dependent IFN-β promoter activity.
A Novel Synthetic Compound, YH-1118, Inhibited LPS-Induced Inflammatory Response by Suppressing IkappaB Kinase/NF-kappaB Pathway in Raw 264.7 Cells.
Lee et al., Inch'ŏn, South Korea. In J Microbiol Biotechnol, Jul 2015
For the search of a potent first-in-class compound to inactivate macrophages responsible for inflammatory responses, in the present study, we investigated the anti-inflammatory effects of YH-1118, a novel synthetic compound, in a lipopolysaccharide (LPS)-stimulated mouse macrophage cell line, Raw 264.7.
[Battle with herpes for 37 years].
Shimomura, In Nihon Ganka Gakkai Zasshi, Mar 2015
IkappaB kinase-β (IKK2) inhibitors, which inhibit the activity of NF-κB, were used to examine gene expression during HSV reactivation in a mouse model.
MiR-199a inhibits the angiogenic potential of endometrial stromal cells under hypoxia by targeting HIF-1α/VEGF pathway.
Di et al., Shanghai, China. In Int J Clin Exp Pathol, 2014
We previously reported that miR-199a suppressed the invasiveness of endometrial stromal cells (ESCs) by targeting IkappaB kinase beta (IKKβ).
Platelet-activating factor: a role in preterm delivery and an essential interaction with Toll-like receptor signaling in mice.
Hirsch et al., Chicago, United States. In Biol Reprod, 2014
In peritoneal macrophages, the PTAFR agonist carbamyl PAF induces production of inflammatory markers previously demonstrated to be upregulated during bacterially induced labor, including: inducible nitric oxide synthase (Nos2), the chemokine Ccl5 (RANTES), tumor necrosis factor (Tnf), and level of their end-products (NO, CCL5, TNF) in a process dependent upon both IkappaB kinase and calcium/calmodulin-dependent protein kinase II.
Hepatic tissue environment in NEMO-deficient mice critically regulates positive selection of donor cells after hepatocyte transplantation.
Streetz et al., Aachen, Germany. In Plos One, 2013
The deletion of the I-kappa B kinase-regulatory subunit IKKγ/NEMO in hepatocytes prevents nuclear factor (NF)-kB activation and triggers spontaneous liver apoptosis, chronic hepatitis and the development of liver fibrosis and hepatocellular carcinoma.
A20-mediated negative regulation of canonical NF-κB signaling pathway.
Shembade et al., Miami, United States. In Immunol Res, 2013
All known NF-κB activators converge on the IkappaB kinase (IKK) complex to activate the canonical and non-canonical NF-κB pathways.
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.
share on facebooktweetadd +1mail to friends