Key features and details
- Rabbit polyclonal to NF-kB p65 (phospho S536)
- Suitable for: WB, IHC-P
- Reacts with: Human
- Isotype: IgG
- Research with confidence – consistent and reproducible results with every batch
- Long-term and scalable supply – powered by recombinant technology for fast production
- Success from the first experiment – confirmed specificity through extensive validation
- Ethical standards compliant – production is animal-free
Product nameAnti-NF-kB p65 (phospho S536) antibody
See all NF-kB p65 primary antibodies
DescriptionRabbit polyclonal to NF-kB p65 (phospho S536)
NF-kappaB p65 (Phospho-Ser536) Antibody detects endogenous levels of NF-kappaB p65 only when phosphorylated at serine536. Suitable treatment will increase the expression - treatment with Calyculin A + TNF-alpha.
Tested applicationsSuitable for: WB, IHC-Pmore details
Species reactivityReacts with: Human
Synthetic peptide corresponding to NF-kB p65 (C terminal) (phospho S536).
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Constituents: PBS, 50% Glycerol (glycerin, glycerine), 0.87% Sodium chloride
Without Mg2+ and Ca2+
Concentration information loading...
PurityImmunogen affinity purified
Purification notesThe antibody against non-phosphopeptide was removed by chromatography using non-phosphopeptide corresponding to the phosphorylation site.
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab28856 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
1/500 - 1/1000. Predicted molecular weight: 60 kDa.
1/50 - 1/100.
1/500 - 1/1000. Predicted molecular weight: 60 kDa.
1/50 - 1/100.
FunctionNF-kappa-B is a pleiotropic transcription factor which is present in almost all cell types and is involved in many biological processed 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 and the heterodimeric p65-p50 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. 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. NF-kappa-B heterodimeric p65-p50 and p65-c-Rel complexes are transcriptional activators. The NF-kappa-B p65-p65 complex appears to be involved in invasin-mediated activation of IL-8 expression. The inhibitory effect of I-kappa-B upon NF-kappa-B the cytoplasm is exerted primarily through the interaction with p65. p65 shows a weak DNA-binding site which could contribute directly to DNA binding in the NF-kappa-B complex. Associates with chromatin at the NF-kappa-B promoter region via association with DDX1.
Sequence similaritiesContains 1 RHD (Rel-like) domain.
Domainthe 9aaTAD motif is a transactivation domain present in a large number of yeast and animal transcription factors.
modificationsUbiquitinated, leading to its proteasomal degradation. Degradation is required for termination of NF-kappa-B response.
Monomethylated at Lys-310 by SETD6. Monomethylation at Lys-310 is recognized by the ANK repeats of EHMT1 and promotes the formation of repressed chromatin at target genes, leading to down-regulation of NF-kappa-B transcription factor activity. Phosphorylation at Ser-311 disrupts the interaction with EHMT1 without preventing monomethylation at Lys-310 and relieves the repression of target genes.
Phosphorylation at Ser-311 disrupts the interaction with EHMT1 and promotes transcription factor activity (By similarity). Phosphorylation on Ser-536 stimulates acetylation on Lys-310 and interaction with CBP; the phosphorylated and acetylated forms show enhanced transcriptional activity.
Reversibly acetylated; the acetylation seems to be mediated by CBP, the deacetylation by HDAC3. Acetylation at Lys-122 enhances DNA binding and impairs association with NFKBIA. Acetylation at Lys-310 is required for full transcriptional activity in the absence of effects on DNA binding and NFKBIA association. Acetylation can also lower DNA-binding and results in nuclear export. Interaction with BRMS1 promotes deacetylation of 'Lys-310'.
Cellular localizationNucleus. Cytoplasm. Nuclear, but also found in the cytoplasm in an inactive form complexed to an inhibitor (I-kappa-B). Colocalized with RELA in the nucleus upon TNF-alpha induction.
- Information by UniProt
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All lanes : Anti-NF-kB p65 (phospho S536) antibody (ab28856)
Lane 1 : K562 cell lysate
Lane 2 : COLO cell lysate
Lane 3 : COLO cell lysate with Phospho Ser536 peptide
Predicted band size: 60 kDa
Paraffin embedded human breast carcinoma stained with ab28856. Left: ab28856, Right: same antibody preincubated with the corresponding synthesized phosphopeptide.
ab28856 has been referenced in 47 publications.
- Ge C et al. Nrf2 deficiency aggravates PM2.5-induced cardiomyopathy by enhancing oxidative stress, fibrosis and inflammation via RIPK3-regulated mitochondrial disorder. Aging (Albany NY) 12:4836-4865 (2020). PubMed: 32182211
- Quinn JA et al. The relationship between members of the canonical NF-kB pathway, tumour microenvironment and cancer specific survival in colorectal cancer patients. Histol Histopathol 35:569-578 (2020). PubMed: 31592535
- Chang CW et al. Fecal Microbiota Transplantation Prevents Intestinal Injury, Upregulation of Toll-Like Receptors, and 5-Fluorouracil/Oxaliplatin-Induced Toxicity in Colorectal Cancer. Int J Mol Sci 21:N/A (2020). PubMed: 31936237
- Pang D et al. Polyphyllin II inhibits liver cancer cell proliferation, migration and invasion through downregulated cofilin activity and the AKT/NF-?B pathway. Biol Open 9:N/A (2020). PubMed: 31988091
- Liu X et al. Multi-walled carbon nanotubes exacerbate doxorubicin-induced cardiotoxicity by altering gut microbiota and pulmonary and colonic macrophage phenotype in mice. Toxicology 435:152410 (2020). PubMed: 32068018
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