Anti-Actin antibody, prediluted (ab15265)
- Product nameAnti-Actin antibody, predilutedSee all Actin primary antibodies ...
- DescriptionRabbit polyclonal to Actin, prediluted
- Tested applicationsWB, IHC-P more details
- Species reactivityReacts with: Mouse, Human
Predicted to work with: Rat, Sheep, Rabbit, Guinea pig, Cow
Synthetic peptide (unfortunately, the amino acid sequence is considered to be commercially sensitive) (Human) (N terminal).
- Positive controlSkeletal muscle.
- Storage instructionsStore at +4°C. Do not freeze.
- Storage bufferPreservative: 0.1% Sodium Azide
Constituents: 1% BSA, 50mM Tris, pH 7.6
- Concentration information loading...
- PurityImmunogen affinity purified
- Clonality Polyclonal
Our Abpromise guarantee covers the use of ab15265 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||WB: Use at an assay dependent dilution. Detects a band of approximately 42 kDa (predicted molecular weight: 42 kDa).|
|IHC-P||IHC-P: Use at an assay dependent dilution. Ready to use. 10 min at RT. No special pre-treatment is required for the Immunohistochemical staining of formalin/paraffin tissues.|
- 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.
- 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 1 actin 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
Anti-Actin antibody, prediluted images
ab15265 staining skeletal muscle Actin by Immunohistochemistry (Formalin/ PFA fixed paraffin-embedded tissue sections).
Anti-Actin antibody (ab15263) at 1/25 dilution + Raji cell lysate
Predicted band size : 42 kDa
Observed band size : 42 kDa
References for Anti-Actin antibody, prediluted (ab15265)
This product has been referenced in:
- Urso ML et al. Adenosine A3 receptor stimulation reduces muscle injury following physical trauma and is associated with alterations in the MMP/TIMP response. J Appl Physiol 112:658-70 (2012). IHC-Fr ; Mouse . Read more (PubMed: 22114177) »
- Zheng J et al. Protective roles of adenosine A1, A2A, and A3 receptors in skeletal muscle ischemia and reperfusion injury. Am J Physiol Heart Circ Physiol 293:H3685-91 (2007). Read more (PubMed: 17921328) »