Human nuclear factor-κB p65,NF-κB p65 ELISA Kit

Code CSB-E08787h
Size 96T,5×96T,10×96T
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Product Details

Target Name
v-rel reticuloendotheliosis viral oncogene homolog A (avian)
Alternative Names
Avian reticuloendotheliosis viral (v rel) oncogene homolog A ELISA Kit; MGC131774 ELISA Kit; NF kappa B p65delta3 ELISA Kit; nfkappabp65 ELISA Kit; NFkB p65 ELISA Kit; NFKB3 ELISA Kit; Nuclear factor kappaB ELISA Kit; Nuclear Factor NF Kappa B p65 Subunit ELISA Kit; Nuclear factor NF-kappa-B p65 subunit ELISA Kit; Nuclear factor of kappa light polypeptide gene enhancer in B cells 3 ELISA Kit; Nuclear factor of kappa light polypeptide gene enhancer in B-cells 3 ELISA Kit; OTTHUMP00000233473 ELISA Kit; OTTHUMP00000233474 ELISA Kit; OTTHUMP00000233475 ELISA Kit; OTTHUMP00000233476 ELISA Kit; OTTHUMP00000233900 ELISA Kit; p65 ELISA Kit; p65 NF kappaB ELISA Kit; p65 NFkB ELISA Kit; relA ELISA Kit; TF65_HUMAN ELISA Kit; Transcription factor NFKB3 ELISA Kit; Transcription factor p65 ELISA Kit; v rel avian reticuloendotheliosis viral oncogene homolog A (nuclear factor of kappa light polypeptide gene enhancer in B cells 3 (p65)) ELISA Kit; V rel avian reticuloendotheliosis viral oncogene homolog A ELISA Kit; v rel reticuloendotheliosis viral oncogene homolog A (avian) ELISA Kit; V rel reticuloendotheliosis viral oncogene homolog A, nuclear factor of kappa light polypeptide gene enhancer in B cells 3, p65 ELISA Kit
Abbreviation
RELA
Uniprot No.
Species
Homo sapiens (Human)
Sample Types
serum, plasma, tissue homogenates
Detection Range
47 pg/mL-3000 pg/mL
Sensitivity
11.75 pg/mL
Assay Time
1-5h
Sample Volume
50-100ul
Detection Wavelength
450 nm
Research Area
Immunology
Assay Principle
quantitative
Measurement
Sandwich
Precision
Intra-assay Precision (Precision within an assay): CV%<8%
Three samples of known concentration were tested twenty times on one plate to assess.
Inter-assay Precision (Precision between assays): CV%<10%
Three samples of known concentration were tested in twenty assays to assess.
Linearity
To assess the linearity of the assay, samples were spiked with high concentrations of human NF-κB p65 in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.
 SampleSerum(n=4)
1:1Average %88
Range %83-92
1:2Average %101
Range %95-104
1:4Average %102
Range %98-105
1:8Average %95
Range %90-98
Recovery
The recovery of human NF-κB p65 spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section.
Sample TypeAverage % RecoveryRange
Serum (n=5) 9389-96
EDTA plasma (n=4)9591-98
Typical Data
These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.
pg/mlOD1OD2AverageCorrected
30002.751 2.732 2.742 2.618
15001.966 1.876 1.921 1.797
7501.356 1.344 1.350 1.226
3750.790 0.777 0.784 0.660
187.50.421 0.403 0.412 0.288
940.323 0.312 0.318 0.194
470.209 0.196 0.203 0.079
00.125 0.123 0.124  
Troubleshooting
and FAQs
Storage
Store at 2-8°C. Please refer to protocol.
Lead Time
3-5 working days after you place the order, and it takes another 3-5 days for delivery via DHL or FedEx
Description

This human NF-κB p65 ELISA kit employs the quantitative sandwich enzyme immunoassay technique to measure the levels of human NF-κB p65 in different samples, including serum, plasma, or tissue homogenates. The enzyme-substrate chromogenic reaction is also used to amplify the signal and quantify the levels of the analyte through the intensity of the colored product. The color intensity positively correlates with the amount of NF-κB p65 bound in the initial step.

p65, also known as RELA, is one of the five components that form the NF-κB transcription factor family and plays a central role in inflammation and immunity. p65 dimerizes with NF-κB1 (p50) to form the heterodimer NF-κB, which is involved in multiple physiological and pathological gene regulation processes, such as inflammatory response, immune response, cell division, proliferation, and apoptosis. Studies have shown that the expression of NF-κB P65 in liver cancer tissues is higher than that in adjacent tissues, and the key to regulating the function of NF-κB is to inhibit the promoting effect of P65 on liver tumors. It is speculated that blocking the activity of NF-κB P65 can inhibit the differentiation and growth of tumor cells, providing a new idea for clinical treatment.

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 Q&A
Q:

I am interested in the nfkb p 65 ELISA kit.
However, I am little confused about the kit as nfkb is an intracellular transcription factor. It's found in the cytoplasm and when activated, it translocates to the nucleus.
So I want to know what is the indication of measuring this factor in the plasma or serum?
What will this express? What is the difference between nfkb kit and nfkb p65 kit?

A:

The CSB-E08787h kit is designed by taking the reference from https://www.uniprot.org/uniprot/Q04206, which is for p65.
As for intracellular proteins, it is generally not secreted outside the cell, but in some metabolism or pathology, cell aging enrichment can be released to the blood, and it can be detected at this time.
CSB-E12107h is designed for p105 by taking the reference from https://www.uniprot.org/uniprot/P19838

NFkb p65 ELISA Kit and NF-κB ELISA Kit target different proteins, detect different objects and use different antibodies.

Target Background

Function
(From Uniprot)
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
  1. 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
  2. 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
  3. 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
  4. These results delineate a novel role of MKRN2 in negatively regulating NF-kappaB-mediated inflammatory responses, cooperatively with PDLIM2. PMID: 28378844
  5. 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
  6. 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
  7. 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
  8. NF-kappaB-94ins/del ATTG genotype might serve as a novel biomarker and potential target for immune thrombocytopenia PMID: 30140708
  9. 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
  10. 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
  11. 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
  12. 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
  13. downregulation of HAGLROS may alleviate lipopolysaccharide-induced inflammatory injury in WI-38cells via modulating miR-100/NF-kappaB axis. PMID: 29673591
  14. 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
  15. 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
  16. 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
  17. 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
  18. High P65 expression is associated with doxorubicin-resistance in breast cancer. PMID: 29181822
  19. reduced miR-138 expression enhanced the destruction of the cartilage tissues among osteoarthritis patients, mainly through targeting p65. PMID: 28537665
  20. 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
  21. 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
  22. 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
  23. 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
  24. 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
  25. 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
  26. this study shows the age-related reductions in serum IL-12 in healthy nonobese subjects PMID: 28762199
  27. NF-kappaB p65 potentiated tumor growth via suppressing a novel target LPTS PMID: 29017500
  28. p65 siRNA retroviruses could suppress the activation of NFkappaB signal pathway. PMID: 28990087
  29. 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
  30. 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
  31. PAK5-mediated phosphorylation and nuclear translocation of NF-kappaB-p65 promotes breast cancer cell proliferation in vitro and in vivo PMID: 29041983
  32. 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
  33. 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
  34. 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
  35. p65 O-GlcNAcylation promotes lung metastasis of cervical cancer cells by activating CXCR4 expression. PMID: 28681591
  36. 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
  37. 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
  38. High NF-kappa-B p65 expression is associated with resistance to doxorubicin in breast cancer. PMID: 27878697
  39. 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
  40. Studied melatonin's role in cell senescence, autophagy, sirtuin 1 expression and acetylation of RelA in hydrogen peroxide treated SH-SY5Y cells. PMID: 28295567
  41. 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
  42. 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
  43. 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
  44. 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
  45. 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
  46. 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
  47. PU.1 supports TRAIL-induced cell death by inhibiting RelA-mediated cell survival and inducing DR5 expression. PMID: 28362429
  48. 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
  49. The Brd4 acetyllysine-binding protein of RelA is involved in activation of polyomavirus JC. PMID: 27007123
  50. 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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