Anti-RELA Antibody (DPABT-H21147)


Host Species
Antibody Isotype


Application Notes
200ul Steriled Distilled Water
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.


Alternative Names
RELA; v-rel reticuloendotheliosis viral oncogene homolog A (avian); NFKB3, nuclear factor of kappa light polypeptide gene enhancer in B cells 3; transcription factor p65; p65; NF-kappa-B p65delta3
Entrez Gene ID
UniProt ID

Product Background

Activated TLR4 signalling, organism-specific biosystem; Activation of NF-kappaB in B Cells, organism-specific biosystem; Acute myeloid leukemia, organism-specific biosystem; Acute myeloid leukemia, conserved biosystem; Adaptive Immune System, organism-specific biosystem; Adipocytokine signaling pathway, organism-specific biosystem; Adipocytokine signaling pathway, conserved biosystem;


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We offer labeled antibodies using our catalogue antibody products and a broad range of intensely fluorescent dyes and labels including HRP, biotin, ALP, Alexa Fluor® dyes, DyLight® Fluor dyes, R-phycoerythrin (R-PE), at scales from less than 100 μg up to 1 g of IgG antibody. Learn More

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Reduced microRNA 375 in colorectal cancer upregulates metadherin-mediated signaling


Authors: Han, Seol-Hee; Mo, Ji-Su; Park, Won-Cheol; Chae, Soo-Cheon

BACKGROUND The human microRNA 375 (MIR375) is significantly downregulated in human colorectal cancer (CRC) and we have previously shown that MIR375 is a CRC-associated miRNA. The metadherin (MTDH) is a candidate target gene of MIR375. AIM To investigate the interaction and function between MIR375 and MTDH in human CRC. METHODS A luciferase reporter system was used to confirm the effect of MIR375 on MTDH expression. The expression levels of MIR375 and the target genes were evaluated by quantitative RT-PCR (qRT-PCR), western blotting, or immunohistochemistry. RESULTS MTDH expression was found to be upregulated in human CRC tissues compared to that in healthy controls. We show that MIR375 regulates the expression of many genes involved in the MTDH-mediated signal transduction pathways [BRAF-MAPK and phosphatidylinositol-4,5-biphosphate-3-kinase catalytic subunit alpha (PIK3CA)-AKT] in CRC cells. Upregulated MTDH expression levels were found to inhibit NF-kappa B inhibitor alpha, which further upregulated NFKB1 and RELA expression in CRC cells. CONCLUSION Our findings suggest that suppressing MIR375 expression in CRC regulates cell proliferation and angiogenesis by increasing MTDH expression. Thus, MIR375 may be of therapeutic value in treating human CRC.

Protective Effect of PBCA Nanoparticles Loaded with Thymulin Against the Relapsing-Remitting Form of Experimental Autoimmune Encephalomyelitis in Mice


Authors: Lunin, Sergey M.; Khrenov, Maxim O.; Glushkova, Olga V.; Parfenyuk, Svetlana B.; Novoselova, Tatyana V.; Novoselova, Elena G.

Relapsing-remitting experimental autoimmune encephalomyelitis (rEAE) in mice is a model that closely resembles relapsing-remitting multiple sclerosis in humans. This study aims to investigate a new approach to modulation of the inflammatory response in rEAE mice using a thymic peptide thymulin bound to polybutylcyanoacrylate (PBCA) nanoparticles. PBCA nanoparticles were used to prolong the presence of thymulin in the blood. Cytokine levels in blood were measured by ELISA; NF-kappa B and SAPK/JNK cascade activation, as well as Hsp72 and p53 protein expression, were measured by Western blotting. Animal health statuses were estimated using severity scores. Results showed that the cytokine response in rEAE was multi-staged: an early phase was accompanied by an increase in plasma interferon-gamma, while the interleukin (IL)-17 response was markedly increased at a later stage. The stages were attributed to rEAE induction and maintenance phases. Thymulin significantly alleviated symptoms of rEAE and lowered plasma cytokine levels both in early and later stages of rEAE, and decreased NF-kappa B and SAPK/JNK cascade activation. Thymulin modulated NF-kappaB pathway activity via site-specific phosphorylation of RelA/p65 protein (at Ser276 and Ser536). The effect of nanoparticle-bound thymulin was more pronounced than the effect of free thymulin. Therefore, PBCA-thymulin can be considered a prospective treatment for this pathology.

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