A synthetic peptide corresponding to residues near the N-terminus of human Actin.
A431 cell lysate; HeLa cells; human cardiac muscle
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents
We are constantly working hard to ensure we provide our customers with best in class antibodies. As a result of this work we are pleased to now offer this antibody in purified format. We are in the process of updating our datasheets. The purified format is designated 'PUR' on our product labels. If you have any questions regarding this update, please contact our Scientific Support team.
This product is a recombinant rabbit monoclonal antibody.
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Avoid freeze / thaw cycle.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Flow Cyt: 1/20.
ICC/IF: 1/250 - 1/500.
IHC-P: 1/100 - 1/200.
IHC-FoFr: 1/500 (PMID 18835925).
WB: 1/1000. Detects a band of approximately 42 kDa (predicted molecular weight: 42 kDa).
Not yet tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
Actins are highly conserved proteins that are involved in various types of cell motility and are ubiquitously expressed in all eukaryotic cells.
Involvement in disease
Defects 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, actin, 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.
Belongs to the actin family.
Oxidation of Met-46 by MICALs (MICAL1, MICAL2 or MICAL3) to form methionine sulfoxide promotes actin filament depolymerization. Methionine sulfoxide is produced stereospecifically, but it is not known whether the (S)-S-oxide or the (R)-S-oxide is produced.
Overlay histogram showing HeLa cells stained with ab46805 (red line). The cells were fixed with 80% methanol (5 min) and then permeabilized with 0.1% PBS-Tween for 20 min. The cells were then incubated in 1x PBS / 10% normal goat serum / 0.3M glycine to block non-specific protein-protein interactions followed by the antibody (ab46805, 1/100 dilution) for 30 min at 22ºC. The secondary antibody used was DyLight® 488 goat anti-rabbit IgG (H+L) (ab96899) at 1/500 dilution for 30 min at 22ºC. Isotype control antibody (black line) was rabbit IgG (monclonal) (1µg/1x106 cells) used under the same conditions. Acquisition of >5,000 events was performed. This antibody gave a positive signal in HeLa cells fixed with 4% paraformaldehyde (10 min)/permeabilized with 0.1% PBS-Tween for 20 min used under the same conditions.
Fluorescent immunohistochemical analysis of paraffin-embedded human smooth muscle tissue using ab46805. Green-specific fluorescent staining.
Immunohistochemistry (Frozen sections) - Anti-muscle Actin antibody [EP184E] (ab46805)Image from Akimoto Y et al., Clin Proteomics. 2011 Sep 21;8(1):15. Fig 3.; doi:10.1186/1559-0275-8-15; 21 September 2011, Clinical Proteomics 2011, 8:15
Immunohistochemical analysis of rat kidney tubule tissue, staining muscle Actin with ab46805.
This product has been referenced in:
He D et al. Apolipoprotein A-1 mimetic peptide 4F promotes endothelial repairing and compromises reendothelialization impaired by oxidized HDL through SR-B1. Redox Biol15:228-242 (2018).
Read more (PubMed: 29277016) »
Song T et al. CRL4 antagonizes SCFFbxo7-mediated turnover of cereblon and BK channel to regulate learning and memory. PLoS Genet14:e1007165 (2018).
Read more (PubMed: 29370161) »