RELA (Ab-276) Antibody
Shipped with Ice Packs 
In Stock 
Description
Western Blot (WB)
The antibody is validated for detecting phosphorylated RelA in whole-cell lysates and nuclear extracts. For example, in HeLa cells treated with tumor necrosis factor (TNF), it successfully identifies RelA phosphorylation at Ser276, which correlates with activation of pro-inflammatory genes like IL-8 and Gro-β .
Immunohistochemistry (IHC)
The antibody is used to localize phosphorylated RelA in tissue sections. Studies with human kidney and lung carcinoma tissues demonstrate its specificity for nuclear RelA in regions of active inflammation .
Immunoprecipitation (IP)
IP experiments reveal interactions between phosphorylated RelA and transcriptional coactivators such as P-TEFb (positive transcription elongation factor b), which is essential for transcriptional elongation of target genes .
Role in NF-κB-Dependent Gene Activation
Phosphorylation of RelA at Ser276 is required for activation of a subset of NF-κB-dependent genes, including IL-8 and Gro-β, but not IκBα . This modification enables RelA to recruit P-TEFb, which phosphorylates RNA polymerase II (Pol II) and facilitates transcriptional elongation.
| Gene | Dependence on Ser276 Phosphorylation |
|---|---|
| IL-8 | High dependence |
| Gro-β | High dependence |
| IκBα | Independent of Ser276 phosphorylation |
Crosstalk with Acetylation
Ser276 phosphorylation is coupled with Lys310 acetylation, enhancing RelA’s interaction with chromatin and coactivators . The antibody has been instrumental in demonstrating that these PTMs are interdependent and critical for inflammatory gene expression.
Validation and Cross-Reactivity
Product Specs
Form
Supplied at 1.0mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Lead Time
We typically ship products within 1-3 business days after receiving your order. Delivery times may vary depending on the purchase method and location. For specific delivery times, please consult your local distributors.
Synonyms
Avian reticuloendotheliosis viral (v rel) oncogene homolog A antibody; MGC131774 antibody; NF kappa B p65delta3 antibody; nfkappabp65 antibody; NFkB p65 antibody; NFKB3 antibody; Nuclear factor kappaB antibody; Nuclear Factor NF Kappa B p65 Subunit antibody; Nuclear factor NF-kappa-B p65 subunit antibody; Nuclear factor of kappa light polypeptide gene enhancer in B cells 3 antibody; Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3 antibody; OTTHUMP00000233473 antibody; OTTHUMP00000233474 antibody; OTTHUMP00000233475 antibody; OTTHUMP00000233476 antibody; OTTHUMP00000233900 antibody; p65 antibody; p65 NF kappaB antibody; p65 NFkB antibody; relA antibody; TF65_HUMAN antibody; Transcription factor NFKB3 antibody; Transcription factor p65 antibody; v rel avian reticuloendotheliosis viral oncogene homolog A (nuclear factor of kappa light polypeptide gene enhancer in B cells 3 (p65)) antibody; V rel avian reticuloendotheliosis viral oncogene homolog A antibody; v rel reticuloendotheliosis viral oncogene homolog A (avian) antibody; V rel reticuloendotheliosis viral oncogene homolog A, nuclear factor of kappa light polypeptide gene enhancer in B cells 3, p65 antibody
Target Names
Uniprot No.
Target Background
Function
NF-κB is a versatile transcription factor found in nearly all cell types. It serves as the endpoint of numerous signal transduction pathways triggered by diverse stimuli, impacting critical biological processes like inflammation, immunity, differentiation, cell growth, tumorigenesis, and apoptosis. NF-κB exists as a homo- or heterodimeric complex composed of Rel-like domain-containing proteins: RELA/p65, RELB, NFKB1/p105, NFKB1/p50, REL, and NFKB2/p52. The RELA-NFKB1 heterodimer is generally the most abundant complex. These dimers bind to κB sites within the DNA of their target genes, exhibiting distinct preferences for various κB sites with varying affinity and specificity. Different dimer combinations can act as transcriptional activators or repressors. For example, the NF-κB heterodimers RELA-NFKB1 and RELA-REL function as transcriptional activators.
NF-κB is regulated by various mechanisms including post-translational modifications, subcellular compartmentalization, and interactions with cofactors or corepressors. NF-κB complexes remain inactive in the cytoplasm, bound to members of the NF-κB inhibitor (I-κB) family. In a conventional activation pathway, I-κB is phosphorylated by I-κB kinases (IKKs) in response to diverse activators. This phosphorylation triggers I-κB degradation, liberating the active NF-κB complex, which then translocates to the nucleus. The inhibitory effect of I-κB on NF-κB, preventing nuclear entry, is primarily mediated by its interaction with RELA. RELA possesses a weak DNA-binding site, potentially contributing to DNA binding within the NF-κB complex.
Beyond its direct transcriptional activator role, RELA can modulate promoter accessibility to transcription factors, indirectly regulating gene expression. RELA associates with chromatin at the NF-κB promoter region through interaction with DDX1. It is crucial for cytokine gene expression in T-cells. The NF-κB homodimeric RELA-RELA complex seems to play a role in invasin-mediated activation of IL-8 expression. Notably, RELA is a key transcription factor regulating the interferon response during SARS-CoV-2 infection.
NF-κB is regulated by various mechanisms including post-translational modifications, subcellular compartmentalization, and interactions with cofactors or corepressors. NF-κB complexes remain inactive in the cytoplasm, bound to members of the NF-κB inhibitor (I-κB) family. In a conventional activation pathway, I-κB is phosphorylated by I-κB kinases (IKKs) in response to diverse activators. This phosphorylation triggers I-κB degradation, liberating the active NF-κB complex, which then translocates to the nucleus. The inhibitory effect of I-κB on NF-κB, preventing nuclear entry, is primarily mediated by its interaction with RELA. RELA possesses a weak DNA-binding site, potentially contributing to DNA binding within the NF-κB complex.
Beyond its direct transcriptional activator role, RELA can modulate promoter accessibility to transcription factors, indirectly regulating gene expression. RELA associates with chromatin at the NF-κB promoter region through interaction with DDX1. It is crucial for cytokine gene expression in T-cells. The NF-κB homodimeric RELA-RELA complex seems to play a role in invasin-mediated activation of IL-8 expression. Notably, RELA is a key transcription factor regulating the interferon response during SARS-CoV-2 infection.
Gene References Into Functions
- These results suggest that resveratrol induces chondrosarcoma cell apoptosis via a SIRT1-activated NF-κB (p65 subunit of NF-κB complex) deacetylation and exhibits anti-chondrosarcoma activity in vivo. PMID: 28600541
- Enhanced IL-1β production by the v65Stop mutant is due in part to induction of DNA binding and the transcriptional activity of NF-κB. 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-κB to the proximal GOT2 promoter are important. PMID: 29666362
- These results delineate a novel role of MKRN2 in negatively regulating NF-κB-mediated inflammatory responses, cooperatively with PDLIM2. PMID: 28378844
- compared with patients with NF-κB-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-κB 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-κB-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-κB signaling pathway..lutein treatment decreased NF-κB signaling pathway related NF-κB 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-κB 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-κB 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-κB 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-κB p65/miR17/RB pathway. As NF-κB 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-κB pathway and c-Met expression PMID: 29039556
- ghrelin effectively suppressed TNF-α-induced inflammatory factors' (including ICAM-1, VCAM-1, MCP-1, and IL-1β) expression through inhibiting AMPK phosphorylation and p65 expression both in HUVEC and THP-1. PMID: 28653238
- these data indicated that the MALAT1/miR146a/NF-κB 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-κB 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-κB 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-κB 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-κB-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-κB-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-κB 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-κB 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 α (TNFα)-induced IκBa phosphorylation, translocation of p65, and expression of NFκB-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-κB 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-κB signaling pathway, and miR-125b acts as oncogene, whereas A20 functions as tumor suppressor. PMID: 28569771
- NF-κB physically interacts with FOXM1 and promotes transcription of FOXM1 gene. NF-κB directly binds FOXM1 gene promoter. Silencing p65 attenuates FOXM1 and beta-catenin expression. NF-κB activation is required for nuclear translocation of FOXM1 and beta-catenin. FOXM1 and beta-catenin positively regulate NF-κB.Knockdown of beta-catenin and FOXM1 downregulates p65 protein and NF-κB-dependent reporte... PMID: 27492973
- PTX treatment of THP-1 macrophages for 1 h induced marked intranuclear translocation of NF-κB 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-κB-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-κB/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 TNFα cooperatively promoted the motility of HCC cells mainly through NF-κB/p65 mediated synergistic induction of FN in vitro. These findings highlight the crosstalk between EGF and TNFα 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-κB p65 pathway, promotes occupancy of the MUC1-C/NF-κB complex on the DNMT1 promoter and drives DNMT1 transcription PMID: 27259275
Database Links
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.
Quick Inquiry
Personal Email Detected
Please use an institutional or corporate email address for inquiries. Personal email accounts ( such as Gmail, Yahoo, and Outlook) are not accepted. *
