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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, beta

IkappaBbeta, IkB
The protein encoded by this gene belongs to the NF-kappa-B inhibitor family, which inhibit NF-kappa-B by complexing with, and trapping it in the cytoplasm. Phosphorylation of serine residues on these proteins by kinases marks them for destruction via the ubiquitination pathway, thereby allowing activation of the NF-kappa-B, which translocates to the nucleus to function as a transcription factor. Alternatively spliced transcript variants have been found for this gene.[provided by RefSeq, Jul 2011] (from NCBI)
Top mentioned proteins: NF-kappaB, IkappaBalpha, p65, V1a, CAN
Papers on IkappaBbeta
Nanostructured lipid carrier mediates effective delivery of methotrexate to induce apoptosis of rheumatoid arthritis via NF-κB and FOXO1.
Katare et al., Chandīgarh, India. In Int J Pharm, Feb 2016
The greater expression of pro-apoptotic gene Bim regulated by NF-κB-IkB and FOXO1 is supported by fold regulations calculated for various apoptotic and pro-inflammatory biomarkers carried out by RT-PCR.
Melatonin, bone regulation and the ubiquitin-proteasome connection: A review.
Reiter et al., Winnipeg, Canada. In Life Sci, Jan 2016
The ubiquitin ligases that are reported to be of major significance in regulating these pathways are the ubiquitin SCF(B-TrCP) ligase (which regulates activation of NF-κB via degradation of IkBα in osteoclasts, and regulates bone transcription factors via degradation of β-catenin), the Keap-Cul3-Rbx1 ligase (which regulates degradation of IkB kinase, Nrf2, and the antiapoptotic factor Bcl-2), and Smurf1.
Decreased expression of TIPE2 contributes to the hyper-reactivity of monocyte to TLR ligands in primary biliary cirrhosis.
Zhong et al., Shanghai, China. In J Gastroenterol Hepatol, Jan 2016
Furthermore, TIPE2 knockdown could promote activation of NF-KB pathways through increasing phosphorylation, degradation of IKB in peripheral blood monocytes from PBC patients.
Differentiation therapy: a promising strategy for cancer treatment.
Liu et al., Guangzhou, China. In Ai Zheng, Dec 2015
The restoration of IkB kinase α (IKKα) leads to the differentiation of nasopharyngeal carcinoma cells with reduced tumorigenicity.
[Qinghuachang Decoction Inhibited NF-kappaB Activation in LPS-induced Human Enterocytes].
Speerra et al., In Zhongguo Zhong Xi Yi Jie He Za Zhi, Nov 2015
There was no obvious change in IKB-alphaB expressions (P > 0.05).
The Keap1-Nrf2-antioxidant response element pathway: a review of its regulation by melatonin and the proteasome.
Reiter et al., Winnipeg, Canada. In Mol Cell Endocrinol, Mar 2015
The ligase (E3) complex (Keap1-Cul3-Rbx1) responsible for ubiquitinating Nrf2, prior to proteasomal degradation, also ubiquitinates IkB kinase and the antiapoptotic factor Bcl-2, and possibly additional proteins.
Transactivation of ErbB Family of Receptor Tyrosine Kinases Is Inhibited by Angiotensin-(1-7) via Its Mas Receptor.
Benter et al., Kuwait, Kuwait. In Plos One, 2014
Ang-(1-7) or AG825 treatment inhibited diabetes-induced phosphorylation of ErbB2 receptor at tyrosine residues Y1221/22, Y1248, Y877, as well as downstream signaling via ERK1/2, p38 MAPK, ROCK, eNOS and IkB-α in the mesenteric vascular bed.
Proteasome inhibitors in progressive renal diseases.
Coppo, Torino, Italy. In Nephrol Dial Transplant, 2014
PS proteolysis is crucial for the degradation of the inhibitory protein IkB of nuclear factor kB (NF-kB), and hence, an interesting field of research has been developed on possible benefits of drugs with anti-PS activity in disease conditions with hyper-expression of NF-kB.
Nuclear factor-κB (NF-κB) inhibitory protein IκBβ determines apoptotic cell death following exposure to oxidative stress.
Dennery et al., Aurora, United States. In J Biol Chem, 2012
Findings represent a necessary but not sufficient role of IkappaBbeta in preventing oxidant stress-induced cell death.
CUEDC2: an emerging key player in inflammation and tumorigenesis.
Zhang et al., Beijing, China. In Protein Cell, 2011
CUEDC2 is also known to interact with IkB kinase α (IKKα) and IKKβ and has an inhibitory role in the activation of transcription factor nuclear factor-κB.
Harnessing the tumor suppressor function of FOXO as an alternative therapeutic approach in cancer.
Khosravi-Far et al., Boston, United States. In Curr Drug Targets, 2011
As substrates that are negatively regulated by oncogenic signaling cascades driven by AKT, SGK (serum- and glucocorticoid-inducible kinase), IkB kinase (IKK), ERK, and cyclin-dependent kinases (CDK), forkhead box-class O (FOXO) transcription factors have emerged as bona fide tumor suppressors.
IkappaBbeta is an essential co-activator for LPS-induced IL-1beta transcription in vivo.
Schmid et al., München, Germany. In J Exp Med, 2010
IkappaBbeta is an essential co-activator for LPS-induced IL-1beta transcription in vivo.
IkappaBbeta acts to inhibit and activate gene expression during the inflammatory response.
Ghosh et al., New Haven, United States. In Nature, 2010
IkappaBbeta acts through p65:c-Rel dimers to maintain prolonged expression of TNF-alpha
A new regulatory mechanism of NF-kappaB activation by I-kappaBbeta in cancer cells.
Kim et al., South Korea. In J Mol Biol, 2009
increased I-kappaBbeta expression reversed NF-kappaB activation in cancer cells, compensating for the loss of I-kappaBalpha via TGase 2 polymerization.
Polymorphisms in NF-kappaB inhibitors and risk of epithelial ovarian cancer.
Goode et al., Rochester, United States. In Bmc Cancer, 2008
NFKBIA and NFKBIB are not likely to harbor ovarian cancer risk alleles.
RSUME, a small RWD-containing protein, enhances SUMO conjugation and stabilizes HIF-1alpha during hypoxia.
Arzt et al., Buenos Aires, Argentina. In Cell, 2007
RSUME enhances the sumoylation of IkB in vitro and in cultured cells, leading to an inhibition of NF-kB transcriptional activity.
c-Rel-dependent priming of naive T cells by inflammatory cytokines.
Sen et al., Waltham, United States. In Immunity, 2005
In resting naive cells c-Rel is associated primarily with IkappaBbeta, an inhibitory molecule that is not effectively degraded by TCR signals.
Distinct roles of IkappaB proteins in regulating constitutive NF-kappaB activity.
Verma et al., Los Angeles, United States. In Nat Cell Biol, 2005
We show that in cells depleted of IkappaBalpha, IkappaBbeta and IkappaBepsilon proteins, a small fraction of p65 binds DNA and leads to constitutive activation of NF-kappaB target genes, even without stimulation, whereas most of the p65 remains cytoplasmic.
Modulation of Th1 activation and inflammation by the NF-kappaB repressor Foxj1.
Peng et al., Saint Louis, United States. In Science, 2004
Foxj1 suppressed NF-kappaB transcription activity in vitro, and Foxj1-deficient T cells possessed increased NF-kappaB activity in vivo, correlating with the ability of Foxj1 to regulate IkappaB proteins, particularly IkappaBbeta.
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