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Read our guarantee »Products:Signal Transduction >> Cytoskeleton / ECM >> Cytoskeleton >> Motor Proteins >> Myosin
Anti-non-muscle Myosin IIA antibody
See all non-muscle Myosin IIA products (7) ...
Mouse monoclonal to non-muscle Myosin IIA
IP, WB, Flow Cyt, ICC/IFmore details
Reacts with
Human
Recombinant fragment: RLKQLKRQLE EAEEEAQRAN ASRRKLQREL EDATETADAM NREVSSLKNK LRRGDLPFVV PRRMARKGAG DGSDEEVDGK ADGAEAKPAE , corresponding to amino acids 131-221 of Human non-muscle Myosin IIA
RLKQLKRQLE EAEEEAQRAN ASRRKLQREL EDATETADAM NREVSSLKNK LRRGDLPFVV PRRMARKGAG DGSDEEVDGK ADGAEAKPAE
Liquid
Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles.
Preservative: None
PBS, pH 7.2
Concentration information loading...
Protein G purified
Monoclonal
IgG2b
kappa
Signal Transduction >> Cytoskeleton / ECM >> Cytoskeleton >> Motor Proteins >> Myosin
Our Abpromise guarantee covers the use of ab55456 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
IP: Use at an assay dependent concentration. (PubMed: 22136066)
WB: Use a concentration of 1 - 5 µg/ml.Detects a band of approximately 215,250 kDa.
Flow Cyt: Use 1µg for 106 cells.
ICC/IF: Use at an assay dependent dilution. (PubMed: 19454694Detection limit: 0.03ng/ml when used as capture antibody against recombinant immunogen.)
Cellular myosin that appears to play a role in cytokinesis, cell shape, and specialized functions such as secretion and capping.
In the kidney, expressed in the glomeruli. Also expressed in leukocytes.
Defects 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).
Contains 1 IQ domain.
Contains 1 myosin head-like domain.
The rodlike tail sequence is highly repetitive, showing cycles of a 28-residue repeat pattern composed of 4 heptapeptides, characteristic for alpha-helical coiled coils.
ISGylated.
Target information above from: UniProt accessionP35579
The UniProt Consortium
The Universal Protein Resource (UniProt) in 2010
Nucleic Acids Res. 38:D142-D148 (2010).
Western blot - non-muscle Myosin IIA antibody (ab55456)

Western blot against tagged recombinant protein immunogen using ab55456 non-muscle Myosin IIA antibody at 1ug/ml. Predicted band size of immunogen is 33 kDa
Immunocytochemistry/ Immunofluorescence-non-muscle Myosin IIA antibody(ab55456)

ICC/IF image of ab55456 stained HeLa cells. The cells were 100% methanol fixed (5 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab55456, 1µg/ml) overnight at +4°C. The secondary antibody (green) was Alexa Fluor® 488 goat anti-mouse IgG (H+L) used at a 1/1000 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.
Flow Cytometry - non-muscle Myosin IIA antibody (ab55456)

Overlay histogram showing HEK293 cells stained with ab55456 (red line). The cells were fixed with 4% paraformaldehyde (10 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 (ab55456, 1µg/1x106 cells) for 30 min at 22°C. The secondary antibody used was DyLight® 488 goat anti-mouse IgG (H+L) (ab96879) at 1/500 dilution for 30 min at 22°C. Isotype control antibody (black line) was mouse IgG2b [PLPV219] (ab91366, 2µg/1x106 cells) used under the same conditions. Acquisition of >5,000 events was performed. This antibody gave a positive signal in HEK293 cells fixed with 100% methanol (5 min)/permeabilized in 0.1% PBS-Tween used under the same conditions.
This product has been referenced in:
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Western blot against tagged recombinant protein immunogen using ab55456 non-muscle Myosin IIA antibody at 1ug/ml. Predicted band size of immunogen is 33 kDa

ICC/IF image of ab55456 stained HeLa cells. The cells were 100% methanol fixed (5 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab55456, 1µg/ml) overnight at +4°C. The secondary antibody (green) was Alexa Fluor® 488 goat anti-mouse IgG (H+L) used at a 1/1000 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.

Overlay histogram showing HEK293 cells stained with ab55456 (red line). The cells were fixed with 4% paraformaldehyde (10 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 (ab55456, 1µg/1x106 cells) for 30 min at 22°C. The secondary antibody used was DyLight® 488 goat anti-mouse IgG (H+L) (
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