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Key Documents

MAB1628

Sigma-Aldrich

Anti-Myosin Antibody, slow muscle, clone NOQ7.5.4D

clone NOQ7.5.4D, Chemicon®, from mouse

Synonym(s):

Anti-CMD1S, Anti-CMH1, Anti-MPD1, Anti-MYHCB, Anti-SPMD, Anti-SPMM

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About This Item

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

biological source

mouse

Quality Level

100

antibody form

purified immunoglobulin

antibody product type

primary antibodies

clone

NOQ7.5.4D, monoclonal

species reactivity

rat, feline, human

manufacturer/tradename

Chemicon®

technique(s)

immunohistochemistry: suitable
radioimmunoassay: suitable
western blot: suitable

isotype

IgG

NCBI accession no.

NM_000257.2

UniProt accession no.

P12883

shipped in

wet ice

target post-translational modification

unmodified

Gene Information

human ... MYH7B(57644)

Specificity

Slow myosin heavy chain. Clearly identifies Type 1 fibers. Within skeletal muscle MAB1628 is specific for slow myosin heavy chain in a wide variety of species. It reacts strongly with rat and feline slow myosin heavy chain. MAB1628 also identifies beta (slow) myosin heavy chain in heart ventricles.

Immunogen

Epitope: slow muscle
Myosin purified from myofibrils isolated from histochemically mixed human skeletal muscle.

Application

Anti-Myosin Antibody, slow muscle, clone NOQ7.5.4D is an antibody against Myosin for use in RIA, WB, IH.
Immunohistochemistry: frozen and formalin fixed sections.

Immunoblotting

RIA

Optimal working dilutions must be determined by end user.

Physical form

Format: Purified

Other Notes

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

Legal Information

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

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Storage Class Code

10 - Combustible liquids

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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Camila Silva Foresto et al.
Journal of applied physiology (Bethesda, Md. : 1985), 121(3), 646-660 (2016-07-23)
Muscle loss occurs following injury and immobilization in adulthood and childhood, which impairs the rehabilitation process; however, far fewer studies have been conducted analyzing atrophic response in infants. This work investigated first the morphological and molecular mechanisms involved in immobilization-induced
Jenny Lund et al.
PloS one, 12(4), e0175441-e0175441 (2017-04-14)
Physical activity has preventive as well as therapeutic benefits for overweight subjects. In this study we aimed to examine effects of in vivo exercise on in vitro metabolic adaptations by studying energy metabolism in cultured myotubes isolated from biopsies taken
Christian M Girgis et al.
Journal of cachexia, sarcopenia and muscle, 10(6), 1228-1240 (2019-06-22)
It has long been recognized that vitamin D deficiency is associated with muscle weakness and falls. Vitamin D receptor (VDR) is present at very low levels in normal muscle. Whether vitamin D plays a direct role in muscle function is
Jeffrey D Covington et al.
Obesity (Silver Spring, Md.), 23(12), 2414-2420 (2015-11-06)
The purpose of the study was to determine the effects of passaging on retention of donor phenotypic characteristics in primary human myotubes. Primary muscle cultures and serial passaged myotubes from physically active, sedentary lean, and individuals with type 2 diabetes
Paola Valdivieso et al.
Frontiers in physiology, 8, 993-993 (2018-01-10)
The insertion/deletion polymorphism in the gene for the regulator of vascular tone, angiotensin-converting enzyme (ACE), is the prototype of a genetic influence on physical fitness and this involves an influence on capillary supply lines and dependent aerobic metabolism in skeletal
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