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Merck

SAB4502610

Anti-NF-κB p65 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

NACRES:
NA.41
UNSPSC Code:
12352203

Nom du produit

Anti-NF-κB p65 antibody produced in rabbit, affinity isolated antibody

biological source

rabbit

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.

Q04206

UniProt accession no.

Q04206

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

unmodified

Quality Level

100

Gene Information

human ... RELA(5970)

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.

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.

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

Physical form

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

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Classe de stockage

10 - Combustible liquids

wgk

nwg

flash_point_f

Not applicable

flash_point_c

Not applicable

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Certificats d'analyse (COA)

Lot/Batch Number
217169

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Retrouvez la documentation relative aux produits que vous avez récemment achetés dans la Bibliothèque de documents.

Consulter la Bibliothèque de documents

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
Chaojie He et al.
European journal of histochemistry : EJH, 68(2) (2024-04-30)
Sepsis-induced myocardial dysfunction (SIMD) is associated with poor prognosis and increased mortality in patients with sepsis. Cytokines are important regulators of both the initiation and progression of sepsis. Interleukin-15 (IL-15), a pro-inflammatory cytokine, has been linked to protective effects against
Dong Ji et al.
Experimental and therapeutic medicine, 14(5), 4910-4918 (2017-12-05)
As a therapeutic target for neuropathic pain, the anti-nociceptive effects of α 2-adrenoceptors (α2AR) have attracted attention. Dexmedetomidine (DEX), a potent and highly selective α2AR agonist, has exhibited significant analgesic effects in neuropathic pain, but the underlying mechanism has remained
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