MAB1645
Anti-Dystrophin Antibody, clone 1808
clone 1808, Chemicon®, from mouse
Synonym(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
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
biological source
mouse
Quality Level
antibody form
purified antibody
antibody product type
primary antibodies
clone
1808, monoclonal
species reactivity
chicken, mouse, rat, human
manufacturer/tradename
Chemicon®
technique(s)
immunohistochemistry: suitable
western blot: suitable
isotype
IgG1
NCBI accession no.
UniProt accession no.
shipped in
dry ice
target post-translational modification
unmodified
Gene Information
human ... DMD(1756)
Specificity
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.
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.
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.
Immunohistochemistry
Optimal working dilutions must be determined by the end user.
Physical form
Format: Purified
Liquid in 0.02 M phosphate buffer (pH 7.6), 250 mM NaCl with 0.1% sodium azide.
Storage and Stability
Maintain at -20ºC for up to 12 months in convenient aliquots. Avoid repeated freeze/thaw cycles.
Legal Information
CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany
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Description
Pricing
WGK
WGK 2
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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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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