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Human p65 Protein expressed in HEK-293 Cells - ABIN2730698
Srinivasan, Blackburn, Lahiri: Functional characterization of a competitive peptide antagonist of p65 in human macrophage-like cells suggests therapeutic potential for chronic inflammation. in Drug design, development and therapy 2015
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Human p65 Protein expressed in Wheat germ - ABIN1317783
Ba, Bacsi, Luo, Aguilera-Aguirre, Zeng, Radak, Brasier, Boldogh: 8-oxoguanine DNA glycosylase-1 augments proinflammatory gene expression by facilitating the recruitment of site-specific transcription factors. in Journal of immunology (Baltimore, Md. : 1950) 2014
In the present study, high levels of CC motif ligand 19 (CCL19), signaling pathways such as Tolllike receptor 4 (TLR4)/nuclear factorkappaB (NFkappaB), and proinflammatory factors including interleukin6 (IL6) and tumor necrosis factora (TNFa) were detected in Nonalcoholic fatty liver disease patients
subjects carrying RelA rs11820062 A allele had a significantly increased risk of hepatitis C virus susceptibility
findings suggested that Sam68 contributed to the production of inflammatory cytokines, proliferation, migration, and invasion of Rheumatoid Arthritis (RA) Fibroblast-like Synoviocytes (FLS( through the NF-kappaB P65 signal transduction pathway and underscored the importance of Sam68 in the inflammation process of RA.
AIRE and p65 bind to P-TEFb independently of BRD4.
These results suggest that resveratrol induces chondrosarcoma cell apoptosis via a SIRT1-activated NF-kappaB (p65 subunit of NF-kappaB complex)deacetylation and exhibits anti-chondrosarcoma activity in vivo.
Enhanced IL-1beta production by the v65Stop mutant is due in part to induction of DNA binding and the transcriptional activity of NF-kappaB.
Study utilizing integrative analysis of transcriptomic, metabolomic, and clinical data propose a model of GOT2 transcriptional regulation, in which the cooperative phosphorylation of STAT3 and direct joint binding of STAT3 and p65/NF-kappaB to the proximal GOT2 promoter are important.
HMBG2 overexpression promotes ischemia/reperfusion-induced cell apoptosis through activating the JNK1/2-NF-kappaBp65 signaling in AC16 cardiomyocytes.
These results delineate a novel role of MKRN2 in negatively regulating NF-kappaB-mediated inflammatory responses, cooperatively with PDLIM2.
compared with patients with NF-kappaB-94 ins/del ATTG ins/ins and ins/del, multiple myeloma patients with del/del had the highest myeloma cell ratio
The riboflavin transporter-3 (SLC52A3) 5'-flanking regions contain NF-kappaB p65/Rel-B-binding sites, which are crucial for mediating SLC52A3 transcriptional activity in esophageal squamous cell carcinoma (ESCC) cells.
Akirin-2 can be a novel biomarker in imatinib resistance. Targeting Akirin-2, NFkappaB and beta-catenin genes may provide an opportunity to overcome imatinib resistance in CML.
NF-kappaB-94ins/del ATTG genotype might serve as a novel biomarker and potential target for immune thrombocytopenia
The results of the present study suggested that the therapeutic effect of TGP on psoriasis may be mediated by modulation of the p38 MAPK/NFkappaB p65 signaling pathway. The results of the present study contribute to the understanding of the role of TGP in the treatment of psoriasis. The present study provides insights suggesting that p38 MAPK may be a novel regulatory signaling pathway for the treatment of psoriasis.
our results suggest that melatonin may exert anti-tumor activities against thyroid carcinoma by inhibition of p65 phosphorylation and induction of reactive oxygen species. Radio-sensitization by melatonin may have clinical benefits in thyroid cancer.
The effect of lutein antiproliferation was mediated by activation of the NrF2/ARE pathway, and blocking of the NF-kappaB signaling pathway..lutein treatment decreased NF-kappaB signaling pathway related NF-kappaB p65 protein expression.
Furthermore, the present study suggested that SNHG15 may be involved in the nuclear factorkappaB signaling pathway, induce the epithelialmesenchymal transition process, and promote renal cell carcinoma invasion and migration.
This revealed that the overexpression of p65 partially reversed SOX4 downregulation-induced apoptosis. In conclusion, our results demonstrated that inhibition of SOX4 markedly induced melanoma cell apoptosis via downregulation of the NF-kappaB signaling pathway, which thus may be a novel approach for the treatment of melanoma.
downregulation of HAGLROS may alleviate lipopolysaccharide-induced inflammatory injury in WI-38cells via modulating miR-100/NF-kappaB axis.
our observations suggest that the RelA-activation domain and multiple cofactor proteins function cooperatively to prime the RelA-DNA binding domain and stabilize the RelA:DNA complex in cells
The role of the PI3K/Akt/mTOR pathway in inflammatory regulation is independent of the activation of TLRs/NF-kappaB. Cross-talk between PI3K/Akt/mTOR and TLRs/NF-kappaB signaling pathways promote inflammation.
PGE2 downregulates LPS-induced inflammatory responses via the TLR4-NF-kappaB signaling pathway in bovine endometrial epithelial cells.
Results showed that the secretion and expression of inflammatory cytokines increased in a dose-dependent manner in response to acetoacetate and glucose; both drugs also upregulated NF-kappa B p65 and Ikappab-alpha phosphorylation levels.
Hepatic SREBP-1c-mediated lipid synthesis and the NF-kappaB inflammatory pathway were both overinduced in cows with fatty liver.
Cytopathic bovine viral diarrhea virus strain induces immune marker production in bovine cells through the NF-kappaB signaling pathway.
The role of NF-kappaB and C/EBP factors in regulating basal and pathogen-induced expression of both genes from cattle, is investigated.
Altering the extracellular matrix to promote p38 activation in cells on fibronectin suppresses NF-kappaB activation, suggesting a novel therapeutic strategy for treating
full length coding sequence of the cattle transcription factor p65 was isolated and cloned
the pathogen causing subclinical mastitis impairs NF-kappaB activation in MEC thereby severely weakening the immune response,induction of IL-8 and TNFalpha, in the udder
These results confirm that VEGI utilizes NF-kappaB as a pro-survival role factor in endothelial cells.
TRAF6 is a novel NS3-interacting protein that inhibits classical swine fever virus replication via activation of NF-kappaB-signaling pathways.
NF-kappaB signaling pathway was activated by transmissible gastroenteritis virus infection.NF-kappaB has 4 binding sites in the FcRn promoter.
TMZ pretreatment effectively reduced the myocardial damage caused by CME via inhibiting the PDCD4/NF-kappaB/ TNF-alpha pathway in cardiomyocytes.
Transmissible gastroenteritis virus infection activates NF-kappaB.
Zinc finger nuclease in-embryo editing of the RELA locus generated live born domestic pigs with the warthog RELA orthologue, associated with resilience to African Swine Fever.
SIRT1, p53 and NF-kappaB are involved in the control of both the proliferation and the apoptosis of ovarian cells.
Porcine Coro1A is an important immunity related gene that helps to inhibit NF-kB activation during H. parasuis infection.
of pp65RHD spatiotemporal expression system is helpful to regulate NFsmall ka, CyrillicB activity and conquer cell-mediated immunity and could be used for preparation of transgenic pig, contributing to xenotransplantation.
Classical swine fever virus failed to activate nuclear factor-kappa b signaling.
We propose that the variation in RELA identified between the warthog and domestic pig has the potential to underlie the difference between tolerance and rapid death upon African swine fever virus infection.
The characterization of porcine NF-kappaB p65 subunit (pp65), is reported.
NFKB activation may occur during the period of uterine receptivity in both cyclic and pregnant endometrium.
Viral non-structural protein 1 suppressed host TNF-alpha promoter by inhibiting NF-kappaB and Sp1 promoter binding activity.
Rela and Traf3 were both targeted by miR-155-5p.
The mechanism of NLRP3 activation in Kupffer cells of liver fibrosis induced by schistosomiasis japonica was shown to be via NF-kappa B metabolism.
Studied anti-inflammatory effects of ethyl acetate extracts of E. sagittatum (Ying-Yang-Huo) and found it to inhibit toll-like receptor 4(TLR4)/ lymphocyte antigen 96(MD-2) thru the NF-kappaB signal pathway.
Bank1 and NF-kappaB as key regulators in anti-nucleolar antibody development
a novel role of canonical NF-kappaB signaling in pruning of surplus synapses on Purkinje neurons in the cerebellum during development
These results indicate that in RGCs, ANXA1 increases IL-1beta expression by recruiting p65 to the nucleus, which induces cell apoptosis. The obtained results may help the development of a novel treatment strategy against RGCs apoptosis in acute ischemia-reperfusion injury.
YY1 was progressively up-regulated in BV2 microglial cells stimulated with lipopolysaccharide (LPS), which was dependent on the transactivation function of nuclear factor kappa B (NF-kappaB). Furthermore, YY1 knockdown notably inhibited LPS-induced the activation of NF-kappaB signaling and interleukin-6 (IL-6) expression in BV-2cells.
This study reports here an X-ray crystal structure of homodimers comprising the RelA DNA-binding domain containing the Rel homology region (RHR) in NF-kappa B bound to an E-selectin promoter fragment with tandem kappa B sites.
These observations imply that pre-excision step(s) during OGG1 initiated base excision repair evoked by reactive oxygen species facilitates NF-kappaB DNA occupancy and gene expression.
p65/NF-kappaB controls ankyrin-G levels in axon initial segment via a negative feedback loop.
This study demonstrates that the synergistic effect between TLR4 and TLR3 in macrophages is an important determinant in acute lung injury and, more importantly, that TLR3 up-regulation is dependent on TLR4-MyD88-NF-kappaB signaling.
During skeletal development, homozygous knockout of transcription factor RelA (Rela) leads to impaired growth through ectopic apoptosis of chondrocytes, whereas heterozygous knockout of Rela does not alter growth.
NF-kappa B p65 transcriptional activity is regulated by platelet-activating factor in macrophages.
Thalidomide potentiates etoposide-induced apoptosis in murine neuroblastoma by suppressing NF-kappaB.
Pudilan xiaoyan oral liquid prevents LPS-induced respiratory in fl ammation via effects on TLR4/NF-kappaB signaling.
Catalase ameliorates diabetes-induced cardiomyopathy through reduced RelA-mediated transcription of BECN1.
SOD2 expression is ATM- and RelA-dependent, ATM knockdown renders cells sensitive to pro-oxidant exposure, and SOD mimetics partially rescue this sensitivity. Mice with germline deletion of Atm fail to develop mature mammary glands, but using a conditional knockout approach, we determined that Atm deletion significantly diminished the expression of Sod2.
RelA-BRD4 signaling in nonciliated bronchiolar epithelial cells mediates neutrophilic airway inflammation and Respiratory Syncytial disease severity.
A significant decline of p65 level was observed in the brain tissues of hamsters infected with scrapie agent 263K at terminal stage. p65 colocalized with neuronal nuclear protein positive cells but not with glial fibrillary acidic protein positive cells.
EMMPRIN inhibited bFGF-induced IL-6 secretion by reducing the p65 subunit phosphorylation, it might be concluded that bFGF and EMMPRIN crosstalk in their respective signaling pathways.
NF-kappa-B is a ubiquitous transcription factor involved in several biological processes. It is held in the cytoplasm in an inactive state by specific inhibitors. Upon degradation of the inhibitor, NF-kappa-B moves to the nucleus and activates transcription of specific genes. NF-kappa-B is composed of NFKB1 or NFKB2 bound to either REL, RELA, or RELB. The most abundant form of NF-kappa-B is NFKB1 complexed with the product of this gene, RELA. Four transcript variants encoding different isoforms have been found for this gene.
C-Rel proto-oncogene protein
, oncogene REL, avian reticuloendotheliosis
, proto-oncogene c-Rel
, v-rel reticuloendotheliosis viral oncogene homolog
, NF-kappa-B p65delta3
, nuclear factor NF-kappa-B p65 subunit
, nuclear factor of kappa light polypeptide gene enhancer in B-cells 3
, transcription factor p65
, v-rel reticuloendotheliosis viral oncogene homolog A
, C-Rel protein
, NF-kappaB transcription factor p65 subunit
, v-rel reticuloendotheliosis viral oncogene homolog A, nuclear factor of kappa light polypeptide gene enhancer in B-cells 3, p65
, nuclear factor kappa B subunit p65
, avian reticuloendotheliosis viral (v-rel) oncogene homolog A
, p65 NF kappaB
, p65 NF-kappa B
, p65 NFkB
, NF-kB p65 subunit
, reticuloendotheliosis oncogene
, v-rel avian reticuloendotheliosis viral oncogene homolog
, LOW QUALITY PROTEIN: proto-oncogene c-Rel