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anti-Human p65 Antibodies:
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Human Polyclonal p65 Primary Antibody for ICC, IHC (p) - ABIN3044253
Kan, Zhou, Jin, Yang: Effects of PDTC on NF-?B expression and apoptosis in rats with severe acute pancreatitis-associated lung injury. in International journal of clinical and experimental medicine 2015
Show all 50 Pubmed References
Mouse (Murine) Polyclonal p65 Primary Antibody for WB - ABIN3043315
Li, Chu, Gao, Li: Apoptotic mechanism of MCF-7 breast cells in vivo and in vitro induced by photodynamic therapy with C-phycocyanin. in Acta biochimica et biophysica Sinica 2009
Show all 46 Pubmed References
Human Polyclonal p65 Primary Antibody for WB - ABIN3042741
Leng, Liu, Yang, Cui, Li, Zhu, Xiong, Zhang, Chen: The apoptotic effect and associated signalling of HSP90 inhibitor 17-DMAG in hepatocellular carcinoma cells. in Cell biology international 2012
Show all 46 Pubmed References
Human Polyclonal p65 Primary Antibody for ELISA, IHC (p) - ABIN5693244
Zhang, Chen, Xin, Li, Li, Lin, Geng, Ding: Oligomannurarate sulfate blocks tumor growth by inhibiting NF-kappaB activation. in Acta pharmacologica Sinica 2010
Show all 45 Pubmed References
Human Polyclonal p65 Primary Antibody for WB - ABIN3043699
Ni, Wang, Yan, Tian, Zhao, Wang, Jiang: Histone deacetylase inhibitor, butyrate, attenuates lipopolysaccharide-induced acute lung injury in mice. in Respiratory research 2010
Show all 43 Pubmed References
Human Polyclonal p65 Primary Antibody for ICC, IF - ABIN151596
Starkey, Haidacher, LeJeune, Zhang, Tieu, Choudhary, Brasier, Denner, Tilton: Diabetes-induced activation of canonical and noncanonical nuclear factor-kappaB pathways in renal cortex. in Diabetes 2006
Show all 29 Pubmed References
Human Polyclonal p65 Primary Antibody for FACS, IF (p) - ABIN668961
Jiang, Tian, Fu, Zhu, Hou: Neuroprotective efficacy and therapeutic window of Forsythoside B: in a rat model of cerebral ischemia and reperfusion injury. in European journal of pharmacology 2010
Show all 16 Pubmed References
Human Polyclonal p65 Primary Antibody for ELISA, ICC - ABIN6263616
Yu, Li, Liu, Tian, Yuan, Bai, Wang, Zhang, Ren, Zhang, Li: Fibroblast growth factor 21 (FGF21) ameliorates collagen-induced arthritis through modulating oxidative stress and suppressing nuclear factor-kappa B pathway. in International immunopharmacology 2015
Show all 14 Pubmed References
Human Polyclonal p65 Primary Antibody for IHC, IP - ABIN6711852
Chen, Zhang, Shen, Wang: Effects of the acid polysaccharide fraction isolated from a cultivated Cordyceps sinensis on macrophages in vitro. in Cellular immunology 2010
Show all 12 Pubmed References
Human Monoclonal p65 Primary Antibody for CyTOF, FACS - ABIN252655
Wittmann, Purwar, Hartmann, Gutzmer, Werfel: Human keratinocytes respond to interleukin-18: implication for the course of chronic inflammatory skin diseases. in The Journal of investigative dermatology 2005
Show all 11 Pubmed References
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.
Overexpression of S1PR1 decreased p65 phosphorylation and translocation into the nucleus. Furthermore, we demonstrated that S1PR1 stimulation inhibited Akt-mTOR signaling, which might contribute to activation of autophagy in HPMECs. Thus, our study provides knowledge crucial to better understanding novel mechanisms underlying the S1PR1-mediated attenuation of cytokine amplification in the pulmonary system during influenza
Lcn2 attenuated NF-kappab subunit p65 activation under hypoxia conditions.
mutation or deletion of the TAD did not modify p65-DNA binding stability, suggesting that the p65 TAD generally contributes neither to the assembly of an "enhanceosome," nor to the active removal of p65 from putative specific binding sites.
p65 NFkappaB-mediated p21 activation controls DNA damage-induced myeloid differentiation.
SIRT1 inhibits rheumatoid arthritis fibroblast-like synoviocyte aggressiveness and inflammatory response in rheumatoid arthritis via suppressing p65 NF-kappaB.
High p65 expression promotes esophageal squamous cancer progression.
Ectopic miR-302e remarkably suppressed the luciferase activity and expression of RelA, whereas down-regulation of miR-302e increased RelA luciferase activity and expression
structure-based mutational analysis of GtgA uncovered amino acids that are required for the interaction of GtgA with p65, as well as those that are required for full activity of GtgA in suppressing NF-kappaB activation.
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.
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.
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.
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.
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