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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
A total of 688 common DEGs were identified between survivors and non-survivors of sepsis, and 96 genes were involved in survival networks. The crucial genes Signal transducer and activator of transcription 5A (STAT5A), CCAAT/enhancer-binding protein beta (CEBPB), Myc proto-oncogene protein (MYC), and REL-associated protein (RELA) were identified and showed increased expression in sepsis survivors.
Real-time PCR and western blotting assay were used to measure the expression of XPR1 in tongue squamous cell carcinoma (TSCC) tissues. Expression of XPR1 and p65 in clinical specimens was analyzed using immunohistochemical assay. The function of XPR1 on progression of TSCC was explored using in vitro and in vivo experiments.
these findings support a role for an activated NF-kappaB system in the transcriptional mechanism of inflammatory processes, especially in synovial membrane of patients with advanced osteoarthritis
RELA haploinsufficiency in CD4 lymphoproliferative disease.
these results suggest that ANKRD49 plays an important role in reducing intrinsic apoptosis of GC-1 cells by modulating the NF-kappaB signaling pathway.
These results identify a pathway by which MTDH regulates NF-kappaB p65 induced EMT during colorectal cancer cell metastasis.
data reveal a protective role of NF-kappaB/RelA in modulating human blood vessel homeostasis and map the human vascular transcriptomic landscapes for the discovery of novel therapeutic targets
research findings demonstrate that SIRT6 serves as a tumor suppressor via regulation of the NF-kappaB pathway, which could offer an innovative strategy to treat adrenocortical carcinoma.
the catalytic USP domain of USP48 interacts with the N-terminal region of the Rel homology domain (RHD) of RelA.
Activation of the NF-kappaB pathway alters the phenotype of MSCs in the tracheal aspirates of preterm infants with severe BPD
This work showed that some RELA DNA binding sites varied in activation response following different stimulations and that interaction with more specialized factors could help achieve this stimulus-specific activity
The expression of SP and TRPV1 in intervertebral disc tissues in patients with Degenerative Disc Disease was associated with NF-kappaB activation.
Reveal a previously unrecognized tumor suppressor function of hyperphosphorylated RB in suppressing NF-kappaB activity and PD-L1 expression, promoting cancer immunity.
our results indicate that Columbianadin (CBN) suppressed the LPS-mediated inflammatory response by inhibiting NOD1/NF- kappa B activation. Further investigations are required to determine the mechanisms of action of CBN in the inhibition of NOD signaling: However, CBN may be employed as a therapeutic agent for multiple inflammatory diseases.
Treatment with PFOA did not affect cell migration, but enhanced cell invasion, adhesion and activity of MMP-2 in FTC133 cells. PFOA selectively enhanced the phosphorylation of nuclear factor kappa B (NF-kappaB) p65, as well as induced NF-kappaB nuclear translocation.
findings suggest that resistance to I-BET151 in U937R cells is related to constitutive activation of the NF-kappaB signaling pathway via increased expression of both BRD2 and BRD4. Targeting the NF-kappaB signaling pathway may be an effective therapeutic strategy to enhance or restore the sensitivity to I-BET151 in U937 cells.
results suggest that NF-kappaB p65 is a critical mediator of mild hypothermia, to which cells are exposed as an extracellular environment, and a central inducer of RBM3 expression, which is responsible for preventing cells from apoptosis
Twist1silencing or overexpression combined with ChR treatment did not affect NF-kappaBp65 levels, but also reduced or enhanced EMT and CSLC properties. Importantly, overexpressing Twist1 combined with ChR reversed the effects of NF-kappaBp65 knockdown and ChR.
results concluded that galangin blocked the thrombin-induced MMP-9 expression in SK-N-SH cells via inhibiting c-Src, Pyk2, PKCalpha/betaII/delta, Akt, mTOR, p42/p44 MAPK, JNK1/2, p38 MAPK, FoxO1, c-Jun, and p65 phosphorylation and ultimately attenuated cell migration.
RELA is a master transcriptional regulator of EMT upstream of WNT morphogen, JUN, SNAI1-ZEB1, and interleukin-6 autocrine loops.
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.
NF-kappaB activation was a major contributor to Porcine transmissible gastroenteritis virus infection-induced inflammation, and nonstructural protein 2 (Nsp2) was the key viral protein involved in the regulation of inflammation, with amino acids 1-120 playing a critical role in activating NF-kappaB.
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.
The study suggests that targeting MIAT may protect against cardiomyocytes against hypoxia-reperfusion injury or myocardial ischemia-reperfusion injury via inhibition of cell apoptosis, mediated by NF-kappaB and PUMA signaling pathway.
role of NF-kappaB in the upregulation of cystathionine-gamma-lyase in bladder pain accompanying cystitis
Hypoxia-inducible factor prolyl-4-hydroxylase-1 is a convergent point in the reciprocal negative regulation of NF-kappaB and p53 signaling pathways
Further analysis revealed that Edwardsiella piscicida phosphothreonine lyase promotes the dephosphorylation and ubiquitination of p65 by inhibiting the phosphorylation of mitogen- and stress-activated protein kinase-1 (MSK1) and by inhibiting the phosphorylation of extracellular signal-related kinase 1/2 (ERK1/2), p38alpha, and c-Jun N-terminal kinase (JNK).
western blot results indicated that SH suppressed the phosphorylation of nuclear factor kappalightchainenhancer of activated Bcells (NFkappaB) p65 protein and reduced the degradation of inhibitor of kappa light polypeptide gene enhancer in Bcells alpha protein in vivo and in vitro.
Results show that the DNA-binding cavity in the RelA-p50 heterodimer is open for DNA binding, whereas in the RelA homodimer, it is occluded.
Deficiency in MyD88 was associated with decreased BDNF expression. Furthermore, the authors identified a valid kappaB-binding site in the BDNF promoter, consistent with activation of NF-kappaB induced by inflammation.
Zbtb7a binds to a significant fraction of genomic promoters and enhancers, encompassing many target genes of nuclear factor kappa B p65 .
High NRP1 expression promotes esophageal squamous cancer progression.
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.
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