Product Details

Uniprot No.

Target Names

Alternative Names

Transcription factor p65 (Nuclear factor NF-kappa-B p65 subunit) (Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3), RELA, NFKB3

Species Reactivity

Human

Immunogen

A synthesized peptide derived from Human RELA

Immunogen Species

Homo sapiens (Human)

Conjugate

Non-conjugated

Clonality

Monoclonal

Isotype

Rabbit IgG

Clone No.

38F2

Purification Method

Affinity-chromatography

Concentration

It differs from different batches. Please contact us to confirm it.

Buffer

Rabbit IgG in 10mM phosphate buffered saline , pH 7.4, 150mM sodium chloride, 0.05% BSA, 0.02% sodium azide and 50% glycerol.

Form

Liquid

Tested Applications

ELISA, WB, IF, FC

Recommended Dilution

Application	Recommended Dilution
WB	1:500-1:2000
IF	1:50-1:200
FC	1:50-1:200

Protocols

ELISA Protocol
Western Blotting(WB) Protocol
Immunofluorescence (IF) Protocol
Flow Cytometry (FC) Protocol

Troubleshooting and FAQs

Antibody FAQs

Storage

Upon receipt, store at -20°C or -80°C. Avoid repeated freeze.

Lead Time

Basically, we can dispatch the products out in 1-3 working days after receiving your orders. Delivery time maybe differs from different purchasing way or location, please kindly consult your local distributors for specific delivery time.

Description

RELA, also known as NF-κB p65, serves as a critical transcription factor within the NF-κB signaling pathway, orchestrating cellular responses to inflammation, immune activation, and stress. This protein plays a central role in regulating genes involved in cell survival, proliferation, and inflammatory cascades, making it an essential target for researchers investigating cancer biology, cardiovascular disease, neuroinflammation, and infectious disease mechanisms.

This recombinant monoclonal antibody, clone 38F2, offers the reproducibility and consistency that demanding experimental workflows require. Because recombinant antibodies are produced from defined genetic sequences rather than traditional hybridoma methods, you can expect reliable performance across experiments and between lots—an important consideration when building long-term datasets or establishing standardized protocols in your laboratory.

Validation studies demonstrate robust performance across multiple applications. In western blot analysis, this antibody detects a clear 70 kDa band matching the predicted molecular weight of RELA, with successful detection confirmed in HeLa, THP-1, MCF7, and A549 cell lysates at dilutions between 1:500 and 1:2000. For cellular localization studies, immunofluorescence staining in PC-3 cells reveals the expected nuclear and cytoplasmic distribution pattern characteristic of NF-κB p65. Flow cytometry validation in HeLa cells shows distinct positive signal separation from isotype controls, enabling quantitative analysis of RELA expression at the single-cell level.

The versatility across western blot, immunofluorescence, and flow cytometry applications provides flexibility for researchers examining NF-κB signaling from multiple experimental angles. Whether you're investigating inflammatory pathway activation, tumor microenvironment dynamics, or metabolic regulation, this antibody supports comprehensive characterization of RELA biology in human cell systems.

Usage

For Research Use Only. Not for use in diagnostic or therapeutic procedures.

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Target Background

Function

NF-kappa-B is a pleiotropic transcription factor present in almost all cell types and is the endpoint of a series of signal transduction events that are initiated by a vast array of stimuli related to many biological processes such as inflammation, immunity, differentiation, cell growth, tumorigenesis and apoptosis. NF-kappa-B is a homo- or heterodimeric complex formed by the Rel-like domain-containing proteins RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL and NFKB2/p52. The heterodimeric RELA-NFKB1 complex appears to be most abundant one. The dimers bind at kappa-B sites in the DNA of their target genes and the individual dimers have distinct preferences for different kappa-B sites that they can bind with distinguishable affinity and specificity. Different dimer combinations act as transcriptional activators or repressors, respectively. The NF-kappa-B heterodimeric RELA-NFKB1 and RELA-REL complexes, for instance, function as transcriptional activators. NF-kappa-B is controlled by various mechanisms of post-translational modification and subcellular compartmentalization as well as by interactions with other cofactors or corepressors. NF-kappa-B complexes are held in the cytoplasm in an inactive state complexed with members of the NF-kappa-B inhibitor (I-kappa-B) family. In a conventional activation pathway, I-kappa-B is phosphorylated by I-kappa-B kinases (IKKs) in response to different activators, subsequently degraded thus liberating the active NF-kappa-B complex which translocates to the nucleus. The inhibitory effect of I-kappa-B on NF-kappa-B through retention in the cytoplasm is exerted primarily through the interaction with RELA. RELA shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Beside its activity as a direct transcriptional activator, it is also able to modulate promoters accessibility to transcription factors and thereby indirectly regulate gene expression. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1. Essential for cytokine gene expression in T-cells. The NF-kappa-B homodimeric RELA-RELA complex appears to be involved in invasin-mediated activation of IL-8 expression. Key transcription factor regulating the IFN response during SARS-CoV-2 infection.

Gene References into Functions

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. PMID: 28600541
Enhanced IL-1beta production by the v65Stop mutant is due in part to induction of DNA binding and the transcriptional activity of NF-kappaB. PMID: 30332797
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. PMID: 29666362
These results delineate a novel role of MKRN2 in negatively regulating NF-kappaB-mediated inflammatory responses, cooperatively with PDLIM2. PMID: 28378844
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 PMID: 30211233
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. PMID: 29428966
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. PMID: 29945498
NF-kappaB-94ins/del ATTG genotype might serve as a novel biomarker and potential target for immune thrombocytopenia PMID: 30140708
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. PMID: 29525603
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. PMID: 29336610
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. PMID: 29750422
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. PMID: 29767266
downregulation of HAGLROS may alleviate lipopolysaccharide-induced inflammatory injury in WI-38cells via modulating miR-100/NF-kappaB axis. PMID: 29673591
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 PMID: 29708732
Results show that MKL1 influences the chromatin structure of pro-inflammatory genes. Specifically, MKL1 defined histone H3K4 trimethylation landscape for NF-kappaB dependent transcription. PMID: 28298643
Studied association of SIRT2 and p53/NF-kB p65 signal pathways in preventing high glucose-induced vascular endothelial cell injury. Results demonstrated that SIRT2 overexpression is associated with deacetylation of p53 and NF-kB p65, which inhibits the high glucose induced apoptosis and vascular endothelial cell inflammation response. PMID: 29189925
In conclusion, the spindle cell morphology should be induced by RelA activation (p-RelA S468) by IKKepsilon upregulation in human herpesvirus 8 vFLIP-expressing EA hy926 cells. PMID: 30029010
High P65 expression is associated with doxorubicin-resistance in breast cancer. PMID: 29181822
reduced miR-138 expression enhanced the destruction of the cartilage tissues among osteoarthritis patients, mainly through targeting p65. PMID: 28537665
the present result indicated that vascular smooth proliferation is regulated by activation of the NF-kappaB p65/miR17/RB pathway. As NF-kappaB p65 signalling is activated in and is a master regulator of the inflammatory response, the present findings may provide a mechanism for the excessive proliferation of VSMCs under inflammation during vascular disorders and may identify novel targets for the treatment of vascular ... PMID: 29115381
the results of real-time PCR and western blotting revealed that Huaier extract decreased p65 and c-Met expression and increased IkappaBalpha expression, while paclitaxel increased p65 expression and reduced IkappaBalpha and c-Met expression.The molecular mechanisms may be involved in the inhibition of the NF-kappaB pathway and c-Met expression PMID: 29039556
ghrelin effectively suppressed TNF-alpha-induced inflammatory factors' (including ICAM-1, VCAM-1, MCP-1, and IL-1beta) expression through inhibiting AMPK phosphorylation and p65 expression both in HUVEC and THP-1. PMID: 28653238
these data indicated that the MALAT1/miR146a/NF-kappaB pathway exerted key functions in LPS-induced acute kidney injury (AKI), and provided novel insights into the mechanisms of this therapeutic candidate for the treatment of the disease. PMID: 29115409
Cytosolic AGR2 contributed to cell metastasis ascribed to its stabilizing effect on p65 protein, which subsequently activated the NF-kappaB and facilitated epithelial to mesenchymal transition (EMT). PMID: 29410027
we provide evidence that S100A7 also inhibits YAP expression and activity through p65/NFkappaB-mediated repression of DeltaNp63, and S100A7 represses drug-induced apoptosis via inhibition of YAP. PMID: 28923839
this study shows the age-related reductions in serum IL-12 in healthy nonobese subjects PMID: 28762199
NF-kappaB p65 potentiated tumor growth via suppressing a novel target LPTS PMID: 29017500
p65 siRNA retroviruses could suppress the activation of NFkappaB signal pathway. PMID: 28990087
miR-215 facilitated HCV replication via inactivation of the NF-kappaB pathway by inhibiting TRIM22, providing a novel potential target for HCV infection. PMID: 29749134
acute inflammation after injury initiates important regenerative signals in part through NF-kappaB-mediated signaling that activates neural stem cells to reconstitute the olfactory epithelium; loss of RelA in the regenerating neuroepithelium perturbs the homeostasis between proliferation and apoptosis PMID: 28696292
PAK5-mediated phosphorylation and nuclear translocation of NF-kappaB-p65 promotes breast cancer cell proliferation in vitro and in vivo PMID: 29041983
While 3-methyladenine rescues cell damage. Our data thus suggest that I/R promotes NF-kappaB p65 activity mediated Beclin 1-mediated autophagic flux, thereby exacerbating myocardial injury. PMID: 27857190
Taken together, these data indicate that up-regulation of ANXA4 leads to activation of the NF-kappaB pathway and its target genes in a feedback regulatory mechanism via the p65 subunit, resulting in tumor growth in GBC. PMID: 27491820
p65 is significantly upregulated in BBN-induced high invasive BCs and human BC cell lines. Our studies have also uncovered a new PTEN/FBW7/RhoGDIalpha axis, which is responsible for the oncogenic role of RelA p65 in promotion of human BC cell migration. PMID: 28772241
p65 O-GlcNAcylation promotes lung metastasis of cervical cancer cells by activating CXCR4 expression. PMID: 28681591
We showed that pristimerin suppressed tumor necrosis factor a (TNFalpha)-induced IkappaBa phosphorylation, translocation of p65, and expression of NFkappaB-dependent genes. Moreover, pristimerin decreased cell viability and clonogenic ability of Uveal melanoma (UM)cells. A synergistic effect was observed in the treatment of pristimerin combined with vinblastine, a frontline therapeutic agent, in UM. PMID: 28766683
This study establishes p65 as a novel target of IMP3 in increasing glioma cell migration and underscores the significance of IMP3-p65 feedback loop for therapeutic targeting in GBM. PMID: 28465487
High NF-kappa-B p65 expression is associated with resistance to doxorubicin in breast cancer. PMID: 27878697
in colon cancer cell migration, activin utilizes NFkB to induce MDM2 activity leading to the degradation of p21 in a PI3K dependent mechanism PMID: 28418896
Studied melatonin's role in cell senescence, autophagy, sirtuin 1 expression and acetylation of RelA in hydrogen peroxide treated SH-SY5Y cells. PMID: 28295567
The data demonstrate that miR-125b regulates nasopharyngeal carcinoma cell proliferation and apoptosis by targeting A20/NF-kappaB signaling pathway, and miR-125b acts as oncogene, whereas A20 functions as tumor suppressor. PMID: 28569771
NF-kappaB physically interacts with FOXM1 and promotes transcription of FOXM1 gene. NF-kappaB directly binds FOXM1 gene promoter. Silencing p65 attenuates FOXM1 and beta-catenin expression. NF-kappaB activation is required for nuclear translocation of FOXM1 and beta-catenin. FOXM1 and beta-catenin positively regulate NF-kappaB.Knockdown of beta-catenin and FOXM1 downregulates p65 protein and NF-kappaB-dependent reporte... PMID: 27492973
PTX treatment of THP-1 macrophages for 1 h induced marked intranuclear translocation of NF-kappaB p65. Low-dose PTX inhibited the M2 phenotype and induced the M1 phenotype via TLR4 signaling, suggesting that low-dose PTX can alter the macrophage phenotype, whereas clinical doses can kill cancer cells. These results suggest that the anticancer effects of PTX are due both to its cytotoxic and immunomodulatory activities PMID: 28440494
Sphk1 induced NF-kappaB-p65 activation, increased expression of cyclin D1, shortened the cell division cycle, and thus promoted proliferation of breast epithelial cells. PMID: 27811358
expression of NF-kappaB/p65 has prognostic value in high risk non-germinal center B-cell-like subtype diffuse large B-cell lymphoma. PMID: 28039454
NFKB1 -94insertion/deletion ATTG polymorphism associated with decreased risks for lung cancer, nasopharyngeal carcinoma, prostate cancer, ovarian cancer, and oral squamous cell carcinoma. PMID: 28039461
PU.1 supports TRAIL-induced cell death by inhibiting RelA-mediated cell survival and inducing DR5 expression. PMID: 28362429
EGF and TNFalpha cooperatively promoted the motility of HCC cells mainly through NF-kappaB/p65 mediated synergistic induction of FN in vitro. These findings highlight the crosstalk between EGF and TNFalpha in promoting HCC, and provide potential targets for HCC prevention and treatment. PMID: 28844984
The Brd4 acetyllysine-binding protein of RelA is involved in activation of polyomavirus JC. PMID: 27007123
MUC1-C activates the NF-kappaB p65 pathway, promotes occupancy of the MUC1-C/NF-kappaB complex on the DNMT1 promoter and drives DNMT1 transcription PMID: 27259275

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Involvement in disease

A chromosomal aberration involving C11orf95 is found in more than two-thirds of supratentorial ependymomas. Translocation with C11orf95 produces a C11orf95-RELA fusion protein. C11orf95-RELA translocations are potent oncogenes that probably transform neural stem cells by driving an aberrant NF-kappa-B transcription program (PubMed:24553141).

Subcellular Location

Nucleus. Cytoplasm.

Database Links

HGNC: 9955

OMIM: 164014

KEGG: hsa:5970

STRING: 9606.ENSP00000384273

UniGene: Hs.502875

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Code	CSB-RA566133A0HU
Size	US$210
	Order now
Image	Western Blot Positive WB detected in: Hela whole cell lysate, THP-1 whole cell lysate, MCF7 whole cell lysate, A549 whole cell lysate All lanes: NF-kB p65 antibody at 1:500 Secondary Goat polyclonal to rabbit IgG at 1/50000 dilution Predicted band size: 70 kDa Observed band size: 70 kDa Immunofluorescence staining of PC-3 with CSB-RA566133A0HU at 1:15, counter-stained with DAPI. The cells were fixed in 4% formaldehyde and blocked in 10% normal Goat Serum. The cells were then incubated with the antibody overnight at 4°C. The secondary antibody was Alexa Fluor 496-congugated AffiniPure Goat Anti-Rabbit IgG(H+L). Overlay Peak curve showing Hela cells stained with CSB-RA566133A0HU (red line) at 1:50. The cells were fixed in 4% formaldehyde and permeated by 0.2% TritonX-100. Then 10% normal goat serum to block non-specific protein-protein interactions followed by the antibody (1µg/110⁶cells) for 45min at 4℃. The secondary antibody used was FITC-conjugated Goat Anti-rabbit IgG(H+L) at 1:200 dilution for 35min at 4℃.Control antibody (green line) was rabbit IgG (1µg/110⁶cells) used under the same conditions. Acquisition of >10,000 events was performed.
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RELA Recombinant Monoclonal Antibody

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Target Background