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Nuclear factor of kappa light polypeptide gene enhancer in B-cells 1

NF-kappaB, NF-kappaB,
This gene encodes a 105 kD protein which can undergo cotranslational processing by the 26S proteasome to produce a 50 kD protein. The 105 kD protein is a Rel protein-specific transcription inhibitor and the 50 kD protein is a DNA binding subunit of the NF-kappa-B (NFKB) protein complex. NFKB is a transcription regulator that is activated by various intra- and extra-cellular stimuli such as cytokines, oxidant-free radicals, ultraviolet irradiation, and bacterial or viral products. Activated NFKB translocates into the nucleus and stimulates the expression of genes involved in a wide variety of biological functions. Inappropriate activation of NFKB has been associated with a number of inflammatory diseases while persistent inhibition of NFKB leads to inappropriate immune cell development or delayed cell growth. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Sep 2009] (from NCBI)
Top mentioned proteins: CAN, p65, V1a, Interleukin-6, HAD
Papers using NF-kappaB antibodies
Mammary-specific Ron receptor overexpression induces highly metastatic mammary tumors associated with beta-catenin activation
Waltz Susan E. et al., In Oncogene, 2005
... Constitutive activation of P I3 K-Akt and NF-kappaB during prostate cancer progression in autochthonous transgenic mouse model ...
Papers on NF-kappaB
Profilin-PTEN interaction suppresses NF-kappa B activation via inhibition of IKK phosphorylation.
Manna et al., Hyderābād, India. In Biochem J, Feb 2016
UNASSIGNED: The molecular mechanism of Profilin for its tumour suppressor activity is still unknown.
Long-term azithromycin ameliorates not only airway inflammation but also remodeling in a murine model of chronic asthma.
Kim et al., Seoul, South Korea. In Pulm Pharmacol Ther, Feb 2016
The expression of MAPK/NF-kappaB signal and the level of BRP-39 in the lung decreased remarkably in the OVA/LPS with azithromycin-treated group.
Lupeol inhibits LPS-induced NF-kappa B signaling in intestinal epithelial cells and macrophages, and attenuates acute and chronic murine colitis.
Kim et al., Seoul, South Korea. In Life Sci, Feb 2016
AIMS: Lupeol, a natural pentacyclic triterpene, exhibits anti-inflammatory effects.
Ionizing radiation modulates human macrophages towards a pro-inflammatory phenotype preserving their pro-invasive and pro-angiogenic capacities.
José Oliveira et al., Porto, Portugal. In Sci Rep, Dec 2015
NF-kappaB transcription activation and increased Bcl-xL expression evidenced the promotion of pro-survival activity.
[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
Expressions of inhibitory Kaba protein (IkappaB-alpha), phosphorylated inhibitory Kaba protein (p-lkappaB-alpha), nuclear transcription factor p50 (p50), and nuclear transcription factor ReIA (ReIA) protein were determined by Western blot.
A cytoplasmic NF-κB interacting long noncoding RNA blocks IκB phosphorylation and suppresses breast cancer metastasis.
Song et al., Guangzhou, China. In Cancer Cell, Apr 2015
Here, we identify an NF-KappaB Interacting LncRNA (NKILA), which is upregulated by NF-κB, binds to NF-κB/IκB, and directly masks phosphorylation motifs of IκB, thereby inhibiting IKK-induced IκB phosphorylation and NF-κB activation.
NF-kappaB Signaling Pathways in Neurological Inflammation: A Mini Review.
Yang et al., Taipei, Taiwan. In Front Mol Neurosci, 2014
The NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells) transcription factor family is a pleiotropic regulator of many cellular signaling pathways, providing a mechanism for the cells in response to a wide variety of stimuli linking to inflammation.
Innate Immune Response in Brain, NF-Kappa B Signaling and Cystatins.
Kopitar-Jerala, Ljubljana, Slovenia. In Front Mol Neurosci, 2014
Recently several reports have demonstrated that innate immune response and inflammation have an important role in major neurodegenerative diseases.
Novel drug targets for personalized precision medicine in relapsed/refractory diffuse large B-cell lymphoma: a comprehensive review.
Hassa et al., Zürich, Switzerland. In Mol Cancer, 2014
Several novel potential drug targets have been recently identified such as the BET bromodomain protein (BRD)-4, phosphoribosyl-pyrophosphate synthetase (PRPS)-2, macrodomain-containing mono-ADP-ribosyltransferase (ARTD)-9 (also known as PARP9), deltex-3-like E3 ubiquitin ligase (DTX3L) (also known as BBAP), NF-kappaB inducing kinase (NIK) and transforming growth factor beta receptor (TGFβR).This review highlights the new insights into the molecular basis of relapsed/refractory DLBCL and summarizes the most promising drug targets and experimental treatments for relapsed/refractory DLBCL, including the use of novel agents such as lenalidomide, ibrutinib, bortezomib, pidilizumab, epratuzumab, brentuximab-vedotin or CAR T cells, dual inhibitors, as well as mechanism-based combinatorial experimental therapies.
NF-KappaB in Long-Term Memory and Structural Plasticity in the Adult Mammalian Brain.
Kaltschmidt et al., Bielefeld, Germany. In Front Mol Neurosci, 2014
The transcription factor nuclear factor kappaB (NF-κB) is a well-known regulator of inflammation, stress, and immune responses as well as cell survival.
Bone Tumor Environment as a Potential Therapeutic Target in Ewing Sarcoma.
Heymann et al., Nantes, France. In Front Oncol, 2014
The first part of the review will focus on targeting the bone resorbing function of osteoclasts by means of bisphosphonates or drugs blocking the pro-resorbing cytokine receptor activator of NF-kappa B ligand.
Chronic intermittent hypoxia induces atherosclerosis by NF-κB-dependent mechanisms.
Liu et al., United States. In Biochim Biophys Acta, 2012
P50 gene deletion inhibited vascular wall inflammation, reduced hepatic TNF-alpha level, attenuated the elevation in serum cholesterol level and diminished macrophage foam cell formation induced by CIH+HCD exposure.
Leukotriene B(4) inhibits neutrophil apoptosis via NADPH oxidase activity: redox control of NF-κB pathway and mitochondrial stability.
Arruda et al., Rio de Janeiro, Brazil. In Biochim Biophys Acta, 2012
NADPH oxidase-derived reactive oxygen species are critical to leukotriene B(4) pro-survival effect on neutrophils. This effect also relies on redox modulation of nuclear factor kappaB signaling pathway.
EHMT1 protein binds to nuclear factor-κB p50 and represses gene expression.
Baltimore et al., Kuala Lumpur, Malaysia. In J Biol Chem, 2012
EHMT1 protein binds to nuclear factor-kappaB p50 and represses gene expression.
Risk association between the NF-κB1 -94ins/delATTG promoter polymorphism and inflammatory bowel diseases: a meta-analysis.
Lin et al., Nanjing, China. In Dig Dis Sci, 2012
This meta-analysis indicated that the NF-kappaB1 -94ins/delATTG promoter polymorphism is a risk factor for ulcerative colitis but not Crohn's disease.
The innate immune sensor NLRC3 attenuates Toll-like receptor signaling via modification of the signaling adaptor TRAF6 and transcription factor NF-κB.
Ting et al., Chapel Hill, United States. In Nat Immunol, 2012
NLRC3 inhibited Toll-like receptor (TLR)-dependent activation of the transcription factor NF-kappaB by interacting with the TLR signaling adaptor TRAF6
Cleavage of NIK by the API2-MALT1 fusion oncoprotein leads to noncanonical NF-kappaB activation.
McAllister-Lucas et al., Ann Arbor, United States. In Science, 2011
study shows API2-MALT1 fusion oncoprotein induces proteolytic cleavage of NF-kappaB-inducing kinase (NIK); resulting deregulated NIK activity is associated with constitutive noncanonical NF-kappaB signaling, enhanced B cell adhesion and apoptosis resistance
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
Because of low expression of the transcription factor RelB in untreated macrophages, high p52 expression repressed basal transcription of both canonical and noncanonical NF-kappaB target genes.
The ubiquitin modifying enzyme A20 restricts B cell survival and prevents autoimmunity.
Ma et al., San Francisco, United States. In Immunity, 2010
A20 is a ubiquitin modifying enzyme that restricts NF-kappaB signals and protects cells against tumor necrosis factor (TNF)-induced programmed cell death.
IkappaBbeta acts to inhibit and activate gene expression during the inflammatory response.
Ghosh et al., New Haven, United States. In Nature, 2010
The activation of pro-inflammatory gene programs by nuclear factor-kappaB (NF-kappaB) is primarily regulated through cytoplasmic sequestration of NF-kappaB by the inhibitor of kappaB (IkappaB) family of proteins.
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