RELA (Ab-536) Antibody
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Description
Antibody Characteristics
RELA (Ab-536) is a polyclonal antibody generated against a synthetic peptide corresponding to residues surrounding Ser536 (amino acids 534–538: F-S-S-I-A) of human RELA/NF-κB p65 .
Biological Significance of RELA-Ser536 Phosphorylation
Phosphorylation of RELA at Ser536 is a post-translational modification critical for NF-κB activation. Key roles include:
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Nuclear Translocation: Required for RelA nuclear entry in response to stimuli like TNF-α or angiotensin II .
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Transcriptional Activation: Enhances NF-κB’s ability to recruit coactivators and drive pro-inflammatory or fibrogenic gene expression .
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Disease Relevance: Elevated in fibrotic tissues (e.g., liver, lung, skin) and cancer models .
Western Blot
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Detects a ~65 kDa band in lysates from TNF-α/Calyculin A-treated HT-29 (colon adenocarcinoma) and HeLa (cervical carcinoma) cells .
Immunohistochemistry
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Localizes phosphorylated RELA to cytoplasm and cell membranes in formalin-fixed paraffin-embedded (FFPE) tissues (e.g., ovarian carcinoma) .
Flow Cytometry
Key Research Findings
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Fibrosis Regulation:
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Kinase Specificity:
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Cell-Type Specificity:
Technical Considerations
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Storage: Stable at -20°C in PBS with 50% glycerol; avoid freeze-thaw cycles .
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Dilutions:
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Controls: Preabsorption with blocking peptide abolishes staining, confirming specificity .
Comparative Insights
Limitations and Future Directions
Product Specs
Form
Supplied at 1.0 mg/mL in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150 mM NaCl, 0.02% sodium azide and 50% glycerol.
Lead Time
Typically, we can ship products within 1-3 business days after receiving your order. Delivery times may vary depending on the purchasing method or location. Please consult your local distributors for specific delivery timelines.
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 pleiotropic transcription factor found in nearly all cell types. It acts as the endpoint of a series of signal transduction events initiated by a wide range of stimuli associated with diverse biological processes. These processes include 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 heterodimeric RELA-NFKB1 complex appears to be the most abundant. These dimers bind to κB sites in the DNA of their target genes, with distinct dimers exhibiting varying affinities and specificities for different κB sites. Different dimer combinations act as transcriptional activators or repressors. For example, the NF-κB heterodimeric RELA-NFKB1 and RELA-REL complexes function as transcriptional activators. NF-κB is regulated by various mechanisms involving post-translational modification, subcellular compartmentalization, and interactions with cofactors or corepressors. NF-κB complexes reside in the cytoplasm in an inactive state, bound to members of the NF-κB inhibitor (I-κB) family. In a conventional activation pathway, I-κB undergoes phosphorylation by I-κB kinases (IKKs) in response to different activators. This phosphorylation leads to I-κB degradation, releasing the active NF-κB complex, which translocates to the nucleus. The inhibitory effect of I-κB on NF-κB, by retaining it in the cytoplasm, is primarily mediated through interaction with RELA. RELA possesses a weak DNA-binding site, potentially contributing directly to DNA binding within the NF-κB complex. Besides its function as a direct transcriptional activator, RELA can also modulate promoter accessibility to transcription factors, indirectly regulating gene expression. It associates with chromatin at the NF-κB promoter region through interaction with DDX1. RELA is essential for cytokine gene expression in T cells. The NF-κB homodimeric RELA-RELA complex is believed to play a role in invasin-mediated activation of IL-8 expression. RELA is a crucial transcription factor regulating the IFN response during SARS-CoV-2 infection.
Gene References Into Functions
- These findings suggest that resveratrol induces chondrosarcoma cell apoptosis through a SIRT1-activated NF-κB (p65 subunit of NF-κB complex) deacetylation, exhibiting anti-chondrosarcoma activity in vivo. PMID: 28600541
- The enhanced IL-1β production by the v65Stop mutant is partially attributed to the induction of DNA binding and transcriptional activity of NF-κB. PMID: 30332797
- A study utilizing integrative analysis of transcriptomic, metabolomic, and clinical data proposes a model for GOT2 transcriptional regulation. This model highlights the cooperative phosphorylation of STAT3 and direct joint binding of STAT3 and p65/NF-κB to the proximal GOT2 promoter as crucial factors. PMID: 29666362
- These results delineate a novel role for MKRN2 in negatively regulating NF-κB-mediated inflammatory responses, in cooperation with PDLIM2. PMID: 28378844
- Compared to patients with NF-κB-94 ins/del ATTG ins/ins and ins/del genotypes, multiple myeloma patients with del/del genotype exhibited 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 could be a novel biomarker for imatinib resistance. Targeting Akirin-2, NFκB, and β-catenin genes may provide an opportunity to overcome imatinib resistance in CML. PMID: 29945498
- The NF-κB-94ins/del ATTG genotype might serve as a novel biomarker and potential target for immune thrombocytopenia. PMID: 30140708
- Our findings suggest that melatonin may exert anti-tumor activities against thyroid carcinoma by inhibiting p65 phosphorylation and inducing reactive oxygen species. Radio-sensitization by melatonin could have clinical benefits in thyroid cancer. PMID: 29525603
- The antiproliferative effect of lutein 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, this study suggests that SNHG15 might be involved in the nuclear factor-kappaB signaling pathway, induce the epithelial-mesenchymal transition process, and promote renal cell carcinoma invasion and migration. PMID: 29750422
- This study revealed that the overexpression of p65 partially reversed SOX4 downregulation-induced apoptosis. In conclusion, these results demonstrate that inhibition of SOX4 significantly induced melanoma cell apoptosis via downregulation of the NF-κB signaling pathway, which might represent a novel approach for melanoma treatment. PMID: 29767266
- Downregulation of HAGLROS may alleviate lipopolysaccharide-induced inflammatory injury in WI-38 cells by modulating the 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
- This study investigated the association of SIRT2 and p53/NF-κB 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-κB p65, which inhibits high glucose-induced apoptosis and vascular endothelial cell inflammation response. PMID: 29189925
- In conclusion, the spindle cell morphology appears to be induced by RelA activation (p-RelA S468) through IKKε 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 cartilage tissues among osteoarthritis patients, primarily through targeting p65. PMID: 28537665
- The present results indicate that vascular smooth proliferation is regulated by activation of the NF-κB p65/miR17/RB pathway. As NF-κB p65 signaling is activated in and is a master regulator of the inflammatory response, these 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
- Real-time PCR and western blotting revealed that Huaier extract decreased p65 and c-Met expression and increased IκBα expression, while paclitaxel increased p65 expression and reduced IκBα and c-Met expression. The molecular mechanisms may involve 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 by inhibiting AMPK phosphorylation and p65 expression in both HUVEC and THP-1. PMID: 28653238
- These data indicate that the MALAT1/miR146a/NF-κB pathway plays key roles in LPS-induced acute kidney injury (AKI), providing novel insights into the mechanisms of this therapeutic candidate for treating the disease. PMID: 29115409
- Cytosolic AGR2 contributed to cell metastasis attributed to its stabilizing effect on p65 protein, subsequently activating NF-κB and facilitating epithelial to mesenchymal transition (EMT). PMID: 29410027
- We provide evidence that S100A7 also inhibits YAP expression and activity through p65/NFκB-mediated repression of ΔNp63, and S100A7 represses drug-induced apoptosis via inhibition of YAP. PMID: 28923839
- This study shows age-related reductions in serum IL-12 in healthy non-obese subjects. PMID: 28762199
- NF-κB p65 potentiated tumor growth by suppressing a novel target LPTS. PMID: 29017500
- p65 siRNA retroviruses could suppress the activation of the NFκB 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 disrupts 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 suggest that I/R promotes NF-κB p65 activity mediated by Beclin 1-mediated autophagic flux, thereby exacerbating myocardial injury. PMID: 27857190
- Taken together, these data indicate that upregulation 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/RhoGDIα axis, which is responsible for the oncogenic role of RelA p65 in promoting 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 IκBα 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 the 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
- This study investigated 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 the A20/NF-κB signaling pathway. miR-125b acts as an oncogene, whereas A20 functions as a tumor suppressor. PMID: 28569771
- NF-κB physically interacts with FOXM1 and promotes transcription of the FOXM1 gene. NF-κB directly binds to the FOXM1 gene promoter. Silencing p65 attenuates FOXM1 and β-catenin expression. NF-κB activation is required for nuclear translocation of FOXM1 and β-catenin. FOXM1 and β-catenin positively regulate NF-κB. Knockdown of β-catenin and FOXM1 downregulates p65 protein and NF-κB-dependent reporter... PMID: 27492973
- PTX treatment of THP-1 macrophages for 1 hour 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, while clinical doses can kill cancer cells. These results suggest that the anticancer effects of PTX are due to both 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
- The NFKB1 -94 insertion/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 the 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.
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