Product nameAnti-non-muscle Myosin IIA antibody [EPR8965] (Phycoerythrin)
See all non-muscle Myosin IIA primary antibodies
DescriptionRabbit monoclonal [EPR8965] to non-muscle Myosin IIA (Phycoerythrin)
ConjugationPhycoerythrin. Ex: 488nm, Em: 575nm
Tested applicationsSuitable for: Flow Cytmore details
Species reactivityReacts with: Human
Synthetic peptide (the amino acid sequence is considered to be commercially sensitive) within Human non-muscle Myosin IIA aa 1900 to the C-terminus. The exact sequence is proprietary.
Database link: P35579
- Flow Cytometry: A431 cells
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents
This product is a recombinant rabbit monoclonal antibody.
Storage instructionsShipped at 4°C. Store at 4°C (stable for up to 12 months). Upon delivery aliquot. Store at +4°C. Do Not Freeze. Store In the Dark.
Storage bufferpH: 7.4
Preservative: 0.02% Sodium azide
Constituents: PBS, 1% BSA
Concentration information loading...
- Anti-non-muscle Myosin IIA antibody [EPR8965] (ab138498)
- Anti-non-muscle Myosin IIA antibody [EPR8965] (Alexa Fluor® 488) (ab204675)
- Anti-non-muscle Myosin IIA antibody [EPR8965] (Alexa Fluor® 647) (ab204676)
- Anti-non-muscle Myosin IIA antibody [EPR8965] (HRP) (ab205470)
- Anti-non-muscle Myosin IIA antibody [EPR8965] - BSA and Azide free (ab236073)
Our Abpromise guarantee covers the use of ab211837 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
The cellular localisation of this product has been verified in ICC/IF
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
Overlay histogram showing A431 cells stained with ab211837 (red line). The cells were fixed with 4% formaldehyde and then permeabilized with 90% methanol at -20°C for 15 min. The cells were then incubated in 1x PBS / 10% normal goat serum to block non-specific protein-protein interactions followed by the antibody (ab211837, 1/5000 dilution) for 30 min at 22°C. Isotype control antibody (black line) was rabbit IgG (monoclonal) Phycoerythrin (ab209478) used at the same concentration and conditions as the primary antibody. Unlabelled sample (blue line) was also used as a control. Acquisition of >5,000 events were collected using a 50mW Yellow/Green laser (561nm) and 586/15 bandpass filter.