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MAB1645

Sigma-Aldrich

Anti-Dystrophin Antibody, clone 1808

clone 1808, Chemicon®, from mouse

Synonim(y):

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

Zaloguj sięWyświetlanie cen organizacyjnych i kontraktowych


About This Item

Kod UNSPSC:
12352203
eCl@ss:
32160702
NACRES:
NA.41

pochodzenie biologiczne

mouse

Poziom jakości

forma przeciwciała

purified antibody

rodzaj przeciwciała

primary antibodies

klon

1808, monoclonal

reaktywność gatunkowa

chicken, mouse, rat, human

producent / nazwa handlowa

Chemicon®

metody

immunohistochemistry: suitable
western blot: suitable

izotyp

IgG1

numer dostępu UniProt

Warunki transportu

dry ice

docelowa modyfikacja potranslacyjna

unmodified

informacje o genach

human ... DMD(1756)

Specyficzność

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.

Immunogen

Peripheral membrane proteins extracted from Torpedo postsynaptic membranes.

Zastosowanie

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.

Postać fizyczna

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

Przechowywanie i stabilność

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

Informacje prawne

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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Kod klasy składowania

10 - Combustible liquids

Klasa zagrożenia wodnego (WGK)

WGK 2

Temperatura zapłonu (°F)

Not applicable

Temperatura zapłonu (°C)

Not applicable


Certyfikaty analizy (CoA)

Poszukaj Certyfikaty analizy (CoA), wpisując numer partii/serii produktów. Numery serii i partii można znaleźć na etykiecie produktu po słowach „seria” lub „partia”.

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Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.

Odwiedź Bibliotekę dokumentów

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
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
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
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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