Key features and details
- Produced recombinantly (animal-free) for high batch-to-batch consistency and long term security of supply
- Alexa Fluor® 488 Rabbit monoclonal [EPR8965] to non-muscle Myosin IIA
- Suitable for: ICC/IF
- Reacts with: Human
- Conjugation: Alexa Fluor® 488. Ex: 495nm, Em: 519nm
Related conjugates and formulations
Product nameAlexa Fluor® 488 Anti-non-muscle Myosin IIA antibody [EPR8965]
See all non-muscle Myosin IIA primary antibodies
DescriptionAlexa Fluor® 488 Rabbit monoclonal [EPR8965] to non-muscle Myosin IIA
ConjugationAlexa Fluor® 488. Ex: 495nm, Em: 519nm
Tested applicationsSuitable for: ICC/IFmore details
Species reactivityReacts with: Human
Synthetic peptide within Human non-muscle Myosin IIA. The exact sequence is proprietary.
Database link: P35579
- ICC/IF: HeLa cells.
This product is a recombinant monoclonal antibody, which offers several advantages including:
- - High batch-to-batch consistency and reproducibility
- - Improved sensitivity and specificity
- - Long-term security of supply
- - Animal-free production
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
Alexa Fluor® is a registered trademark of Molecular Probes, Inc, a Thermo Fisher Scientific Company. The Alexa Fluor® dye included in this product is provided under an intellectual property license from Life Technologies Corporation. As this product contains the Alexa Fluor® dye, the purchase of this product conveys to the buyer the non-transferable right to use the purchased product and components of the product only in research conducted by the buyer (whether the buyer is an academic or for-profit entity). As this product contains the Alexa Fluor® dye the sale of this product is expressly conditioned on the buyer not using the product or its components, or any materials made using the product or its components, in any activity to generate revenue, which may include, but is not limited to use of the product or its components: in manufacturing; (ii) to provide a service, information, or data in return for payment (iii) for therapeutic, diagnostic or prophylactic purposes; or (iv) for resale, regardless of whether they are sold for use in research. For information on purchasing a license to this product for purposes other than research, contact Life Technologies Corporation, 5781 Van Allen Way, Carlsbad, CA 92008 USA or firstname.lastname@example.org.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Avoid freeze / thaw cycle. Store In the Dark.
Storage bufferpH: 7.40
Preservative: 0.02% Sodium azide
Constituents: PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
Concentration information loading...
PurityProtein A purified
- Anti-non-muscle Myosin IIA antibody [EPR8965] (ab138498)
- Alexa Fluor® 647 Anti-non-muscle Myosin IIA antibody [EPR8965] (ab204676)
- HRP Anti-non-muscle Myosin IIA antibody [EPR8965] (ab205470)
- PE Anti-non-muscle Myosin IIA antibody [EPR8965] (ab211837)
- Anti-non-muscle Myosin IIA antibody [EPR8965] - BSA and Azide free (ab236073)
The Abpromise guarantee
Our Abpromise guarantee covers the use of ab204675 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
FunctionCellular myosin that appears to play a role in cytokinesis, cell shape, and specialized functions such as secretion and capping.
Tissue specificityIn the kidney, expressed in the glomeruli. Also expressed in leukocytes.
Involvement in diseaseDefects in MYH9 are the cause of May-Hegglin anomaly (MHA) [MIM:155100]. MHA is an autosomal dominant macrothrombocytopenia characterized by thrombocytopenia, giant platelets and leukokyte inclusions appearing as highly parallel paracrystalline bodies.
Defects in MYH9 are the cause of Sebastian syndrome (SBS) [MIM:605249]. SBS is an autosomal dominant macrothrombocytopenia characterized by thrombocytopenia, giant platelets and leukocyte inclusions that are smaller and less organized than in May-Hegglin anomaly.
Defects in MYH9 are the cause of Fechtner syndrome (FTNS) [MIM:153640]. FTNS is an autosomal dominant macrothrombocytopenia characterized by thrombocytopenia, giant platelets and leukocyte inclusions that are small and poorly organized. Additionally, FTNS is distinguished by Alport-like clinical features of sensorineural deafness, cataracts and nephritis.
Defects in MYH9 are the cause of Alport syndrome with macrothrombocytopenia (APSM) [MIM:153650]. APSM is an autosomal dominant disorder characterized by the association of ocular lesions, sensorineural hearing loss and nephritis (Alport syndrome) with platelet defects.
Defects in MYH9 are the cause of Epstein syndrome (EPS) [MIM:153650]. EPS is an autosomal dominant disorder characterized by the association of macrothrombocytopathy, sensorineural hearing loss and nephritis.
Defects in MYH9 are the cause of deafness autosomal dominant type 17 (DFNA17) [MIM:603622]. DFNA17 is a form of sensorineural hearing loss. Sensorineural deafness results from damage to the neural receptors of the inner ear, the nerve pathways to the brain, or the area of the brain that receives sound information. DFNA17 is characterized by progressive hearing impairment and cochleosaccular degeneration.
Defects in MYH9 are the cause of macrothrombocytopenia with progressive sensorineural deafness (MPSD) [MIM:600208]. MPSD is an autosomal dominant disorder characterized by the association of macrothrombocytopathy and progressive sensorineural hearing loss without renal dysfunction.
Note=Subjects with mutations in the motor domain of MYH9 present with severe thrombocytopenia and develop nephritis and deafness before the age of 40 years, while those with mutations in the tail domain have a much lower risk of noncongenital complications and significantly higher platelet counts. The clinical course of patients with mutations in the four most frequently affected residues of MYH9 (responsible for 70% of MYH9-related cases) were evaluated. Mutations at residue 1933 do not induce kidney damage or cataracts and cause deafness only in the elderly, those in position 702 result in severe thrombocytopenia and produce nephritis and deafness at a juvenile age, while alterations at residue 1424 or 1841 result in intermediate clinical pictures.
Note=Genetic variations in MYH9 are associated with non-diabetic end stage renal disease (ESRD).
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.
- Information by UniProt
- BDPLT 6 antibody
- BDPLT6 antibody
- Cellular myosin heavy chain antibody
ab204675 staining non-muscle Myosin IIA in HeLa cells. The cells were fixed with 4% formaldehyde (10 min), permeabilized with 0.1% Triton X-100 for 5 minutes and then blocked with 1% BSA/10% normal goat serum/0.3M glycine in 0.1% PBS-Tween for 1h. The cells were then incubated overnight at +4°C with ab204675 at 1/100 dilution (shown in green) and ab195889, Mouse monoclonal to alpha Tubulin (Alexa Fluor® 594), at 1/250 dilution (shown in red). Nuclear DNA was labelled with DAPI (shown in blue).
Image was taken with a confocal microscope (Leica-Microsystems, TCS SP8).
This product also gave a positive signal under the same testing conditions in HeLa cells fixed with 100% methanol (5 min).
ab204675 has been referenced in 3 publications.
- Cabezas MD et al. Subcellular Control over Focal Adhesion Anisotropy, Independent of Cell Morphology, Dictates Stem Cell Fate. ACS Nano 13:11144-11152 (2019). PubMed: 31532622
- Uttagomol J et al. Evidence for the Desmosomal Cadherin Desmoglein-3 in Regulating YAP and Phospho-YAP in Keratinocyte Responses to Mechanical Forces. Int J Mol Sci 20:N/A (2019). PubMed: 31835537
- Li X et al. Desmoglein-3 acts as a pro-survival protein by suppressing reactive oxygen species and doming whilst augmenting the tight junctions in MDCK cells. Mech Ageing Dev 184:111174 (2019). PubMed: 31678215