Key features and details
- Rabbit polyclonal to Slow Skeletal Myosin Heavy chain - C-terminal
- Suitable for: IHC-P
- Reacts with: Human
- Isotype: IgG
Product nameAnti-Slow Skeletal Myosin Heavy chain antibody - C-terminal
See all Slow Skeletal Myosin Heavy chain primary antibodies
DescriptionRabbit polyclonal to Slow Skeletal Myosin Heavy chain - C-terminal
Tested applicationsSuitable for: IHC-Pmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse, Rat
Recombinant fragment (GST-tag) within Human Slow Skeletal Myosin Heavy chain (C terminal). The exact immunogen sequence used to generate this antibody is proprietary information. If additional detail on the immunogen is needed to determine the suitability of the antibody for your needs, please contact our Scientific Support team to discuss your requirements.
Database link: P12883
- Human colon cancer tissue.
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Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.4
Preservative: 0.05% Sodium azide
Constituents: 50% Glycerol (glycerin, glycerine), 49% PBS
Concentration information loading...
PurityImmunogen affinity purified
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab197687 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
1/10 - 1/50.
1/10 - 1/50.
Tissue specificityBoth wild type and variant Gln-403 are detected in skeletal muscle (at protein level).
Involvement in diseaseDefects in MYH7 are the cause of cardiomyopathy familial hypertrophic type 1 (CMH1) [MIM:192600]. Familial hypertrophic cardiomyopathy is a hereditary heart disorder characterized by ventricular hypertrophy, which is usually asymmetric and often involves the interventricular septum. The symptoms include dyspnea, syncope, collapse, palpitations, and chest pain. They can be readily provoked by exercise. The disorder has inter- and intrafamilial variability ranging from benign to malignant forms with high risk of cardiac failure and sudden cardiac death.
Defects in MYH7 are the cause of myopathy myosin storage (MYOMS) [MIM:608358]. In this disorder, muscle biopsy shows type 1 fiber predominance and increased interstitial fat and connective tissue. Inclusion bodies consisting of the beta cardiac myosin heavy chain are present in the majority of type 1 fibers, but not in type 2 fibers.
Defects in MYH7 are the cause of scapuloperoneal myopathy MYH7-related (SPMM) [MIM:181430]; also known as scapuloperoneal syndrome myopathic type. SPMM is a progressive muscular atrophia beginning in the lower legs and affecting the shoulder region earlier and more severely than distal arm.
Defects in MYH7 are a cause of cardiomyopathy dilated type 1S (CMD1S) [MIM:613426]. Dilated cardiomyopathy is a disorder characterized by ventricular dilation and impaired systolic function, resulting in congestive heart failure and arrhythmia. Patients are at risk of premature death.
Defects in MYH7 are the cause of myopathy distal type 1 (MPD1) [MIM:160500]. MPD1 is a muscular disorder characterized by early-onset selective weakness of the great toe and ankle dorsiflexors, followed by weakness of the finger extensors. Mild proximal weakness occasionally develops years later after the onset of the disease.
Sequence similaritiesContains 1 IQ domain.
Contains 1 myosin head-like domain.
DomainThe rodlike tail sequence is highly repetitive, showing cycles of a 28-residue repeat pattern composed of 4 heptapeptides, characteristic for alpha-helical coiled coils.
Each myosin heavy chain can be split into 1 light meromyosin (LMM) and 1 heavy meromyosin (HMM). It can later be split further into 2 globular subfragments (S1) and 1 rod-shaped subfragment (S2).
Cellular localizationCytoplasm > myofibril. Thick filaments of the myofibrils.
- Information by UniProt
- Beta myosin heavy chain antibody
- cardiac muscle beta isoform antibody
- CMD1S antibody
ab197687 has not yet been referenced specifically in any publications.