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Key Documents

AB9482

Sigma-Aldrich

Anti-Retinoid-Related Orphan Receptor β Antibody

Chemicon®, from rabbit

Synonyme(s) :

ROR Beta/NR

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About This Item

Code UNSPSC :
12352203
eCl@ss :
32160702
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

Forme d'anticorps

affinity purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

polyclonal

Produit purifié par

affinity chromatography

Espèces réactives

human

Fabricant/nom de marque

Chemicon®

Technique(s)

immunohistochemistry: suitable (paraffin)

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

dry ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... RORB(6096)

Spécificité

Recognizes Retinoid-Related Orphan Receptor Beta [ROR Beta/NR].

Immunogène

Synthetic peptide from the hinge domain of human Retinoid-Related Orphan Receptor Beta.

Application

Immunohistochemistry on paraffin embedded tissue sections.

Optimal working dilutions must be determined by the end user.
Research Category
Epigenetics & Nuclear Function
Research Sub Category
Transcription Factors
Use Anti-Retinoid-Related Orphan Receptor β Antibody (Rabbit Polyclonal Antibody) validated in IHC(P) to detect Retinoid-Related Orphan Receptor β also known as ROR Beta/NR.

Forme physique

Affinity purified immunoglobulin. Liquid in PBS, pH 7.7 with 0.01% sodium azide.

Stockage et stabilité

Maintain at -70°C in undiluted aliquots for up to 6 months after date of receipt. Avoid repeated freeze/thaw cycles.

Autres remarques

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

Informations légales

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

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)

WGK 2

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

Consulter la Bibliothèque de documents

Claudia Günther et al.
The Journal of clinical investigation, 126(11), 4346-4360 (2016-11-02)
Although necrosis and necroinflammation are central features of many liver diseases, the role of programmed necrosis in the context of inflammation-dependent hepatocellular death remains to be fully determined. Here, we have demonstrated that the pseudokinase mixed lineage kinase domain-like protein
The pathogenic role of the canonical Wnt pathway in age-related macular degeneration.
Zhou, T; Hu, Y; Chen, Y; Zhou, KK; Zhang, B; Gao, G; Ma, JX
Investigative Ophthalmology & Visual Science null
Contrasting behavior of the p18INK4c and p16INK4a tumor suppressors in both replicative and oncogene-induced senescence.
Gagrica, S; Brookes, S; Anderton, E; Rowe, J; Peters, G
Cancer Research null
Vincent Ricchiuti et al.
The Journal of endocrinology, 211(1), 47-54 (2011-07-13)
Liberal or high-sodium (HS) intake, in conjunction with an activated renin-angiotensin-aldosterone system, increases cardiovascular (CV) damage. We tested the hypothesis that sodium intake regulates the type 1 angiotensin II receptor (AT(1)R), mineralocorticoid receptor (MR), and associated signaling pathways in heart
Yaling Yin et al.
Proceedings of the National Academy of Sciences of the United States of America, 113(26), E3773-E3781 (2016-06-15)
Intracellular accumulation of wild-type tau is a hallmark of sporadic Alzheimer's disease (AD), but the molecular mechanisms underlying tau-induced synapse impairment and memory deficit are poorly understood. Here we found that overexpression of human wild-type full-length tau (termed hTau) induced

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