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MAB5466

Sigma-Aldrich

Anti-Bestrophin Antibody

Chemicon®, from mouse

Synonyme(s) :

Anti-Anti-ARB, Anti-Anti-BEST, Anti-Anti-BMD, Anti-Anti-Best1V1Delta2, Anti-Anti-RP50, Anti-Anti-TU15B, Anti-Anti-VMD2

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About This Item

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

Source biologique

mouse

Niveau de qualité

100

Forme d'anticorps

purified immunoglobulin

Type de produit anticorps

primary antibodies

Clone

monoclonal

Espèces réactives

monkey, pig, mouse, bovine, human

Fabricant/nom de marque

Chemicon®

Technique(s)

immunohistochemistry: suitable
western blot: suitable

Isotype

IgG

Numéro d'accès NCBI

NM_004183.2

Numéro d'accès UniProt

O76090

Conditions d'expédition

dry ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... BEST1(7439)

Spécificité

Reacts with bestrophin.

Immunogène

Recombinant human bestrophin protein.

Application

Detect Bestrophin using this Anti-Bestrophin Antibody validated for use in WB, IH.
Research Category
Neuroscience
Research Sub Category
Neurodegenerative Diseases
Western blot: 5 μg/mL of this antibody detected Bestrophin in bovine retina cell lysate.

Immunohistochemistry (Paraffin) Analysis: A 1:20 dilution from a representative lot detected Bestrophin in mouse retina tissue sections.

Optimal working dilutions must be determined by end user.

Forme physique

Format: Purified
Purified immunoglobulin. Liquid in PBS containing 0.08% sodium azide.

Stockage et stabilité

Maintain at -20°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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Réf. du produit
Description
Tarif

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

Transplantation of human central nervous system stem cells - neuroprotection in retinal degeneration.
Trevor J McGill,Benjamin Cottam,Bin Lu,Shaomei Wang,Sergej Girman,Chunyu Tian et al.
The European Journal of Neuroscience null
Attenuation of choroidal neovascularization by ?(2)-adrenoreceptor antagonism.
Lavine, JA; Sang, Y; Wang, S; Ip, MS; Sheibani, N
JAMA Ophthalmology null
Divya Sinha et al.
American journal of human genetics, 107(2), 278-292 (2020-07-25)
Dominantly inherited disorders are not typically considered to be therapeutic candidates for gene augmentation. Here, we utilized induced pluripotent stem cell-derived retinal pigment epithelium (iPSC-RPE) to test the potential of gene augmentation to treat Best disease, a dominant macular dystrophy
Alvaro Plaza Reyes et al.
Nature communications, 11(1), 1609-1609 (2020-04-02)
In vitro differentiation of human pluripotent stem cells into functional retinal pigment epithelial (RPE) cells provides a potentially unlimited source for cell based reparative therapy of age-related macular degeneration. Although the inherent pigmentation of the RPE cells have been useful
Cynthia Tang et al.
Communications biology, 4(1), 161-161 (2021-02-07)
Mutations in CLN3 lead to photoreceptor cell loss in CLN3 disease, a lysosomal storage disorder characterized by childhood-onset vision loss, neurological impairment, and premature death. However, how CLN3 mutations cause photoreceptor cell death is not known. Here, we show that

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