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Key Documents

SAB4300442

Sigma-Aldrich

Anti-RELA (Ab-505) 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

UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

~65 kDa

species reactivity

human

concentration

1 mg/mL

technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:50-1:100

isotype

IgG

immunogen sequence

(L-V-T-G-A)

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... RELA(5970)

Immunogen

Peptide sequence around aa. 503-507 (L-V-T-G-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

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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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Schistosomiasis japonica is a serious tropical parasitic disease in humans, which causes inflammation and fibrosis of the liver. Hepatic stellate cells (HSCs) are known to play an important role in schistosome-induced fibrosis, but their role in schistosome-induced inflammation is still
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Clinical science (London, England : 1979), 127(3), 195-208 (2014-02-12)
The TGFβ (transforming growth factor β)/SMAD and NF-κB (nuclear factor κB) signalling pathways play a key role in hypertensive nephropathy. The present study examined whether targeting these pathways by SMAD7, a downstream inhibitor of both pathways, blocks AngII (angiotensin II)-induced

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