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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase beta

IKKbeta, IKK2
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. [provided by RefSeq, Sep 2011] (from NCBI)
Papers using IKKbeta antibodies
The IKK2/NF-{kappa}B pathway suppresses MYC-induced lymphomagenesis
Supplier
Siegmund D et al., In Cell Death & Disease, 2008
... The IKK2 inhibitor TPCA-1 was from Tocris Bioscience (Ellisville, MO, USA) ...
Homotypic and heterotypic interactions of EWS, FLI1 and their oncogenic fusion protein.
Supplier
Agarwal Sudha, In PLoS ONE, 2002
... Antibodies for TRAF1 (H-125), TRAF2 (H-249), IKK2 (H-470) and HA (HA-probe Y-11) were from Santa Cruz Biotechnology Inc; antibodies against the ...
Papers on IKKbeta
Silencing of IkBβ mRNA causes disruption of mitochondrial retrograde signaling and suppression of tumor growth in vivo.
GeneRIF
Avadhani et al., Philadelphia, United States. In Carcinogenesis, 2012
findings demonstrate that IkBbeta is a master regulator of mitochondrial retrograde signaling pathway and that the retrograde signaling plays a role in tumor growth in vivo
Nuclear factor κB activation impairs ependymal ciliogenesis and links neuroinflammation to hydrocephalus formation.
GeneRIF
Baumann et al., Ulm, Germany. In J Neurosci, 2012
This study demonstrated that IKK/NF-kappaB activation is sufficient to induce hydrocephalus formation and provides a potential mechanistic explanation for the frequent association of neuroinflammation and hydrocephalus formation during brain development
Chronic activation of the kinase IKKβ impairs T cell function and survival.
GeneRIF
Zhong et al., Durham, United States. In J Immunol, 2012
Uncontrolled IKKbeta activation promotes T cell apoptosis and attenuates responsiveness to T cell receptor stimulation and bacterial infection in vivo.
Cardiomyocyte-specific IκB kinase (IKK)/NF-κB activation induces reversible inflammatory cardiomyopathy and heart failure.
GeneRIF
Wirth et al., Ulm, Germany. In Proc Natl Acad Sci U S A, 2012
IKK/NF-kappaB activation in cardiomyocytes is sufficient to cause cardiomyopathy and heart failure by inducing an excessive inflammatory response and myocyte atrophy.
A role for the NF-κB pathway in cell protection from complement-dependent cytotoxicity.
GeneRIF
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.
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