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SAB4300009

Sigma-Aldrich

Anti-phospho-RELA (p65/pSer536) antibody produced in rabbit

affinity isolated antibody

Synonym(s):

Anti-MGC131774 antibody produced in rabbit, Anti-NFKB3 antibody produced in rabbit, Anti-p65 antibody produced in rabbit, Anti-v-rel reticuloendotheliosis viral oncogene homolog A (avian) antibody produced in rabbit

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About This Item

MDL number:
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

~65 kDa

species reactivity

rat, mouse, human

concentration

1 mg/mL

technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:50-1:100
indirect immunofluorescence: 1:100-1:200
western blot: 1:500-1:1000

isotype

IgG

immunogen sequence

(F-S-SP-I-A)

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

phosphorylation (pSer536)

Gene Information

human ... RELA(5970)

Immunogen

Peptide sequence around phosphorylation site of serine 536 (F-S-S(p)-I-A), according to the protein RELA.

Features and Benefits

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Target description

NF-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.

Physical form

Solution in phosphate-buffered saline containing 0.02% sodium azide and 50% glycerol

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Le Qin et al.
Molecular medicine (Cambridge, Mass.), 25(1), 28-28 (2019-06-15)
Circular RNAs (circRNAs) contribute to the epigenetic modulation of pathological and physiological conditions. The understanding of the impact of circRNAs on generation of testicular inflammatory reactions is insufficient. Our research adopted a poly I:C-triggered testicular inflammation murine model and cell

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