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Key Documents

SAB4502616

Sigma-Aldrich

Anti-NF-κB p65 (Acetyl-Lys310) antibody produced in rabbit

affinity isolated antibody

Synonyme(s) :

NFKB3, RELA, TF65, nuclear factor NF-κ-B p65 subunit, p65

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About This Item

Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

100

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

antigen 60 kDa

Espèces réactives

mouse, human

Concentration

~1 mg/mL

Technique(s)

ELISA: 1:40000
immunofluorescence: 1:100-1:500
immunohistochemistry: 1:50-1:100
western blot: 1:500-1:1000

Numéro d'accès NCBI

Q04206

Numéro d'accès UniProt

Q04206

Conditions d'expédition

wet ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

acetylation (Lys310)

Informations sur le gène

human ... RELA(5970)

Catégories apparentées

Description générale

Anti-NF-κB p65 (Acetyl-Lys310) Antibody detects endogenous levels of total NF-κB p65 (Acetyl-Lys310) protein.
RELA (v-rel avian reticuloendotheliosis viral oncogene homolog A) codes for the important constituent of the NF-κB (nuclear factor κ-B) complex. It is located on human chromosome 11q13.1. It is also called as nuclear factor κB subunit 3 (NFKB3).

Immunogène

The antiserum was produced against synthesized peptide derived from human NF-kappaB p65 around the acetylated site of Lys310.

Immunogen Range: 275-324

Application

Anti-NF-κB p65 (Acetyl-Lys310) antibody has been used in western blotting.

Actions biochimiques/physiologiques

RELA (v-rel avian reticuloendotheliosis viral oncogene homolog A) participates in nuclear factor κ-B (NFKB) signaling pathway. It also controls inflammation. Alterations in the gene results in schizophrenia and startle reactions.

Caractéristiques et avantages

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.

Forme physique

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.

Clause de non-responsabilité

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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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

nwg

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable

Certificats d'analyse (COA)

Recherchez un Certificats d'analyse (COA) en saisissant le numéro de lot du produit. Les numéros de lot figurent sur l'étiquette du produit après les mots "Lot" ou "Batch".

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Consulter la Bibliothèque de documents

17β-Estradiol Attenuates Hematoma Expansion through ERα/Sirt1/NF-?B Pathway in Hyperglycemic Intracerebral Hemorrhage Mice
Zheng Y, et al.
Stroke, 46(2), 485-485 (2015)
Variants of the RELA gene are associated with schizophrenia and their startle responses.
Hashimoto R, et al.
Neuropsychopharmacology, 36(9), 1921-1921 (2011)
Genome-wide association analysis of soluble ICAM-1 concentration reveals novel associations at the NFKBIK, PNPLA3, RELA, and SH2B3 loci.
Pare G, et al.
PLoS Genetics, 7(4), e1001374-e1001374 (2011)
Yun Zheng et al.
Stroke, 46(2), 485-491 (2014-12-20)
17β-estradiol (E2) has been reported to reduce bleeding and brain injury in experimental intracerebral hemorrhage (ICH) model. However, it is not clear if E2 can prevent early hematoma expansion (HE) induced by hyperglycemia in acute ICH. The aim of this
Chun-Cheih Chao et al.
Cell, 179(7), 1483-1498 (2019-12-10)
Metabolism has been shown to control peripheral immunity, but little is known about its role in central nervous system (CNS) inflammation. Through a combination of proteomic, metabolomic, transcriptomic, and perturbation studies, we found that sphingolipid metabolism in astrocytes triggers the

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