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SAB4502610

Sigma-Aldrich

Anti-NF-κB p65 antibody produced in rabbit

affinity isolated antibody

Sinónimos:

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

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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

antigen 60 kDa

species reactivity

rat, mouse, human

concentration

~1 mg/mL

technique(s)

ELISA: 1:10000
immunofluorescence: 1:100-1:500
immunohistochemistry: 1:50-1:100
western blot: 1:500-1:1000

NCBI accession no.

UniProt accession no.

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Gene Information

human ... RELA(5970)

General description

Anti-NF-κB p65 Antibody detects endogenous levels of total NF-κB p65 protein.

Immunogen

The antiserum was produced against synthesized peptide derived from human NF-kappaB p65.

Immunogen Range: 249-298

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.

Physical form

Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 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

10 - Combustible liquids

wgk_germany

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable


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Certificados de análisis (COA)

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Visite la Librería de documentos

Janelle R Zacherl et al.
Journal of cellular biochemistry, 116(4), 524-532 (2014-11-02)
Artificial trans fatty acids promote atherosclerosis by blocking macrophage clearance of cell debris. Classical fatty-acid response mechanisms include TLR4-NF-κB activation, and Erk1/2 phosphorylation, but these may not indicate long-term mechanisms. Indeed, nuclear NF-κB was increased by 60 min treatment by 30 μM
Zhen Luo et al.
Journal of cellular physiology, 234(4), 3583-3597 (2018-10-27)
Pancreatic ductal adenocarcinoma (PDAC) remains a challenging malignancy due to distant metastasis. RELA, a major component of the NF-κB pathway, could serve as an oncogene through activating proliferation or migration-related gene expression, including NEAT1, a well-known oncogenic long noncoding RNA.
Jiangang Liu et al.
Molecular medicine reports, 17(4), 5065-5073 (2018-02-03)
During the development of postoperative vascular restenosis, the aberrant proliferation of vascular smooth muscle cells (VSMCs) is a critical event resulting in intimal hyperplasia. Inflammatory responses involving the activation of nuclear factor (NF)‑κB are among the major molecular processes underlying
Lili Zhang et al.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 95, 808-817 (2017-09-12)
Previous studies have shown that inflammatory process contributes to the pathogenesis of cardiac damage induced by diabetes mellitus. However, the underlying mechanisms and strategies to alleviate inflammatory injury in the diabetic heart are not fully elucidated. In this study, we
Caroline Martins Sandanielo Marques et al.
Mutation research, 824, 42-51 (2017-11-19)
Glucose, in the presence of reactive oxygen species (ROS), acts as an as an oxidative agent and drives deleterious processes in Diabetes Mellitus. We have studied the mechanism and the toxicological effects of glucose-dependent glycoxidation reactions driven by copper and

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