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MAB1645

Sigma-Aldrich

Anti-Dystrophin Antibody

CHEMICON®, mouse monoclonal, 1808

Synonyme(s) :

Anti-BMD, Anti-CMD3B, Anti-DXS142, Anti-DXS164, Anti-DXS206, Anti-DXS230, Anti-DXS239, Anti-DXS268, Anti-DXS269, Anti-DXS270, Anti-DXS272, Anti-MRX85

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About This Item

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

product name

Anti-Dystrophin Antibody, clone 1808, clone 1808, Chemicon®, from mouse

Source biologique

mouse

Niveau de qualité

100

Forme d'anticorps

purified antibody

Type de produit anticorps

primary antibodies

Clone

1808, monoclonal

Espèces réactives

chicken, mouse, rat, human

Fabricant/nom de marque

Chemicon®

Technique(s)

immunohistochemistry: suitable
western blot: suitable

Isotype

IgG1

Numéro d'accès NCBI

NM_000109.2
NM_004006.1
NM_004007.1
NM_004009.2
NM_004010.2
NM_004011.2
NM_004012.2
NM_004013.1
NM_004014.1
NM_004015.1
NM_004016.1
NM_004017.1
NM_004018.1
NM_004019.2
NM_004020.1
NM_004021.1
NM_004022.1
NM_004023.1

Numéro d'accès UniProt

P11532

Conditions d'expédition

dry ice

Modification post-traductionnelle de la cible

unmodified

Informations sur le gène

human ... DMD(1756)

Spécificité

By Western blot MAB1645 recognizes a single protein having a relative molecular weight of 300 kD. Reacts to mammalian skeletal muscle dystrophin. Shows no staining of mdx mouse muscle. Labels normal human muscle but not Duchenne muscle.

STAINING PATTERN:

On cryostat sections of normal mouse diaphragm MAB1645 gives strong immunofluorescence staining of the entire sarcolemma, with particularly strong staining of neuromuscular junctions.

SPECIES REACTIVITY:

Labels skeletal muscle from rat, chicken and Xenopus laevis. Labels cardiac muscle from rat and normal, but not mdx, mouse. Also labels smooth muscle from chicken gizzard.

Immunogène

Peripheral membrane proteins extracted from Torpedo postsynaptic membranes.

Application

Anti-Dystrophin Antibody, clone 1808 detects level of Dystrophin & has been published & validated for use in WB, IH.
Western blot

Immunohistochemistry

Optimal working dilutions must be determined by the end user.

Forme physique

Format: Purified
Liquid in 0.02 M phosphate buffer (pH 7.6), 250 mM NaCl with 0.1% sodium azide.

Stockage et stabilité

Maintain at -20ºC for up to 12 months in convenient aliquots. Avoid repeated freeze/thaw cycles.

Informations légales

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

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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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Consulter la Bibliothèque de documents

Andreas Schaefer et al.
PloS one, 11(2), e0148259-e0148259 (2016-02-04)
Previous small animal models for simulation of mechanical unloading are solely performed in healthy or infarcted hearts, not representing the pathophysiology of hypertrophic and dilated hearts emerging in heart failure patients. In this article, we present a new and economic
Andreas Schaefer et al.
Scientific reports, 9(1), 5710-5710 (2019-04-07)
Mechanical unloading (MU) by implantation of left ventricular assist devices (LVAD) has become clinical routine. This procedure has been shown to reverse cardiac pathological remodeling, with the underlying molecular mechanisms incompletely understood. Most studies thus far were performed in non-standardized
Mariana Fernandez-Caggiano et al.
Nature metabolism, 2(11), 1223-1231 (2020-10-28)
Cardiomyocytes rely on metabolic substrates, not only to fuel cardiac output, but also for growth and remodelling during stress. Here we show that mitochondrial pyruvate carrier (MPC) abundance mediates pathological cardiac hypertrophy. MPC abundance was reduced in failing hypertrophic human
Tessa R Werner et al.
Scientific reports, 9(1), 11494-11494 (2019-08-09)
Afterload enhancement (AE) of rat engineered heart tissue (EHT) in vitro leads to a multitude of changes that in vivo are referred to as pathological cardiac hypertrophy: e.g., cardiomyocyte hypertrophy, contractile dysfunction, reactivation of fetal genes and fibrotic changes. Moreover
Payam Soltanzadeh et al.
Neuromuscular disorders : NMD, 20(8), 499-504 (2010-07-16)
Manifesting carriers of DMD gene mutations may present diagnostic challenges, particularly in the absence of a family history of dystrophinopathy. We review the clinical and genetic features in 15 manifesting carriers identified among 860 subjects within the United Dystrophinopathy Project
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