Overview
- Product nameAnti-Actin antibodySee all Actin primary antibodies ...
- DescriptionRabbit polyclonal to Actin
- Tested applicationsWB more details
- Species reactivityReacts with: Mouse, Rat, Sheep, Rabbit, Chicken, Guinea pig, Hamster, Cow, Dog, Human, Pig, Xenopus laevis, Monkey
- Immunogen
Full length native protein purified from bovine skeletal muscle
- Positive controlMouse Heart Tissue Extract, Chicken Heart Tissue Extract
Properties
- FormLiquid
- Storage instructionsStore at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze / thaw cycles.
- Storage bufferPreservative: 0.09% Sodium Azide
Constituents: 50% Glycerol, PBS, pH 7.2 -
Concentration information loading... - PurityProtein A purified
- Clonality Polyclonal
- IsotypeIgG
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Research Areas
Applications
Our Abpromise guarantee covers the use of ab69512 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
| Application | Notes |
|---|---|
| WB | WB: 1/1000. Detects a band of approximately 42 kDa (predicted molecular weight: 42 kDa). |
Target
- FunctionActins are highly conserved proteins that are involved in various types of cell motility and are ubiquitously expressed in all eukaryotic cells.
- Involvement in diseaseDefects in ACTA1 are the cause of nemaline myopathy type 3 (NEM3) [MIM:161800]. A form of nemaline myopathy. Nemaline myopathies are muscular disorders characterized by muscle weakness of varying severity and onset, and abnormal thread-or rod-like structures in muscle fibers on histologic examination. The phenotype at histological level is variable. Some patients present areas devoid of oxidative activity containg (cores) within myofibers. Core lesions are unstructured and poorly circumscribed.
Defects in ACTA1 are a cause of myopathy congenital with excess of thin myofilaments (MPCETM) [MIM:161800]. A congenital muscular disorder characterized at histological level by areas of sarcoplasm devoid of normal myofibrils and mitochondria, and replaced with dense masses of thin filaments. Central cores, rods, ragged red fibers, and necrosis are absent.
Defects in ACTA1 are a cause of congenital myopathy with fiber-type disproportion (CFTD) [MIM:255310]; also known as congenital fiber-type disproportion myopathy (CFTDM). CFTD is a genetically heterogeneous disorder in which there is relative hypotrophy of type 1 muscle fibers compared to type 2 fibers on skeletal muscle biopsy. However, these findings are not specific and can be found in many different myopathic and neuropathic conditions. - Sequence similaritiesBelongs to the actin family.
- Cellular localizationCytoplasm > cytoskeleton.
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Database links
- Entrez Gene: 58 Human
- Entrez Gene: 11459 Mouse
- Entrez Gene: 29437 Rat
- Omim: 102610 Human
- SwissProt: P68133 Human
- SwissProt: P68134 Mouse
- SwissProt: P68136 Rat
- Unigene: 1288 Human
- Unigene: 214950 Mouse
- Unigene: 82732 Rat
see all
Target information above from: UniProt accession
P68133
The UniProt Consortium
The Universal Protein Resource (UniProt) in 2010
Nucleic Acids Res. 38:D142-D148 (2010)
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Alternative names
- ACTA antibodyACTA1 antibodyActin alpha skeletal muscle antibody
- Actin antibodyactin, alpha 1, skeletal muscle 1 antibodyactin, alpha 1, skeletal muscle antibodyActin, alpha skeletal muscle antibodyACTS_HUMAN antibodyalpha Actin 1 antibodyalpha skeletal muscle Actin antibodyalpha skeletal muscle antibodyAlpha-actin-1 antibodyASMA antibodyCFTD antibodyCFTD1 antibodyCFTDM antibodyMPFD antibodyNEM1 antibodyNEM2 antibodyNEM3 antibodynemaline myopathy type 3 antibody
see all
Anti-Actin antibody images
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All lanes : Anti-Actin antibody (ab69512) at 1/1000 dilution
Lane 1 : MW marker
Lane 2 : Mouse heart tissue extract
Lane 3 : Chicken heart tissue extract
Predicted band size : 42 kDa
Observed band size : 42 kDa
Additional bands at : 35 kDa,55 kDa,70 kDa. We are unsure as to the identity of these extra bands.
References for Anti-Actin antibody (ab69512)
ab69512 has not yet been referenced specifically in any publications.
