Validated using a knockout cell line
Recombinant
RabMAb

Recombinant Anti-non-muscle Myosin IIA antibody [EPR8965] - BSA and Azide free (ab236073)

Overview

  • Product name
    Anti-non-muscle Myosin IIA antibody [EPR8965] - BSA and Azide free
    See all non-muscle Myosin IIA primary antibodies
  • Description
    Rabbit monoclonal [EPR8965] to non-muscle Myosin IIA - BSA and Azide free
  • Host species
    Rabbit
  • Tested applications
    Suitable for: IHC-P, ICC/IF, Flow Cyt, WBmore details
  • Species reactivity
    Reacts with: Human
  • Immunogen

    Synthetic peptide within Human non-muscle Myosin IIA aa 1900-2000. The exact sequence is proprietary.

  • Positive control
    • WB: HAP1, HeLa and HEK-293 cell lysates.
  • General notes

    The formulation and the concentration of this product is compatible for metal-conjugation for mass cytometry (CyTOF®).

    ab236073 is a PBS-only buffer format of ab138498. Please refer to ab138498 for recommended dilutions, protocols, and image data.

    Mouse, Rat: We have preliminary internal testing data to indicate this antibody may not react with these species. Please contact us for more information.

     

    Use our conjugation kits for antibody conjugates that are ready-to-use in as little as 20 minutes with <1 minute hands-on-time and 100% antibody recovery: available for fluorescent dyes, HRP, biotin and gold.

    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.

Properties

  • Form
    Liquid
  • Storage instructions
    Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
  • Storage buffer
    Constituent: PBS
  • Concentration information loading...
  • Purity
    Affinity purified
  • Clonality
    Monoclonal
  • Clone number
    EPR8965
  • Isotype
    IgG
  • Research areas

Applications

Our Abpromise guarantee covers the use of ab236073 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
IHC-P Use at an assay dependent concentration. Perform heat mediated antigen retrieval before commencing with IHC staining protocol.
ICC/IF Use at an assay dependent concentration.
Flow Cyt Use at an assay dependent concentration.

ab172730 - Rabbit monoclonal IgG, is suitable for use as an isotype control with this antibody.

WB Use at an assay dependent concentration. Detects a band of approximately 230 kDa (predicted molecular weight: 227 kDa).

Target

  • Function
    Cellular myosin that appears to play a role in cytokinesis, cell shape, and specialized functions such as secretion and capping.
  • Tissue specificity
    In the kidney, expressed in the glomeruli. Also expressed in leukocytes.
  • Involvement in disease
    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).
  • Sequence similarities
    Contains 1 IQ domain.
    Contains 1 myosin head-like domain.
  • 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.
  • Post-translational
    modifications
    ISGylated.
  • Information by UniProt
  • Database links
  • Alternative names
    • BDPLT 6 antibody
    • BDPLT6 antibody
    • Cellular myosin heavy chain antibody
    • Cellular myosin heavy chain type A antibody
    • DFNA 17 antibody
    • DFNA17 antibody
    • EPSTS antibody
    • FTNS antibody
    • MGC104539 antibody
    • MHA antibody
    • MYH 2A antibody
    • MYH 9 antibody
    • MYH2A antibody
    • MYH9 antibody
    • MYH9_HUMAN antibody
    • MYHas8 antibody
    • MyHC 2A antibody
    • MyHC IIa antibody
    • MyHC2A antibody
    • MyHCIIa antibody
    • MYHSA 2 antibody
    • MYHSA2 antibody
    • Myosin 9 antibody
    • Myosin heavy chain 9 antibody
    • Myosin heavy chain 9 non muscle antibody
    • Myosin heavy chain antibody
    • Myosin heavy chain non muscle IIa antibody
    • Myosin heavy chain nonmuscle IIa antibody
    • Myosin heavy polypeptide 2 antibody
    • Myosin heavy polypeptide 9 non muscle antibody
    • Myosin-9 antibody
    • Myosin9 antibody
    • NMHC II A antibody
    • NMMHC A antibody
    • NMMHC II a antibody
    • NMMHC II-a antibody
    • NMMHC IIA antibody
    • NMMHC-A antibody
    • NMMHC-IIA antibody
    • NMMHCA antibody
    • Non muscle myosin heavy chain A antibody
    • Non muscle myosin heavy chain antibody
    • Non muscle myosin heavy chain II A antibody
    • Non muscle myosin heavy polypeptide 9 antibody
    • non-muscle IIa antibody
    • Non-muscle myosin heavy chain A antibody
    • Non-muscle myosin heavy chain IIa antibody
    • Nonmuscle myosin heavy chain A antibody
    • Nonmuscle myosin heavy chain II A antibody
    • type A antibody
    see all

Images

  • Lane 1: Wild-type HAP1 cell lysate (20 µg)
    Lane 2: non-muscle Myosin IIA knockout HAP1 cell lysate (20 µg)
    Lane 3: HeLa cell lysate (20 µg)
    Lane 4: HEK293 cell lysate (20 µg)
    Lanes 1 - 4: Merged signal (red and green). Green - ab138498 observed at 230 kDa. Red - loading control, ab18058, observed at 124 kDa.

    ab138498 was shown to specifically react with non-muscle Myosin IIA in wild-type HAP1 cells. No band was observed when non-muscle Myosin IIA knockout samples were examined. Wild-type and non-muscle Myosin IIA knockout samples were subjected to SDS-PAGE. ab138498 at a dilution of 1/1000 and ab18058 (loading control to Vinculin) at a dilution of 1/10,000 were incubated overnight at 4°C. Blots were developed with Goat anti-Rabbit IgG H&L (IRDye® 800CW) preadsorbed (ab216773) and Goat anti-Mouse IgG H&L (IRDye® 680RD) preadsorbed (ab216776) secondary antibodies at 1/10,000 dilution for 1 hour at room temperature before imaging.

    This data was developed using the same antibody clone in a different buffer formulation containing PBS, BSA, glycerol, and sodium azide (ab138498).

  • Immunohistochemical analysis of paraffin embedded Human kidney tissue labelling non-muscle Myosin IIA with ab138498 antibody at a dilution of 1/250.

    This data was developed using the same antibody clone in a different buffer formulation containing PBS, BSA, glycerol, and sodium azide (ab138498).

  • Immunohistochemical analysis of paraffin embedded Human lung tissue labelling non-muscle Myosin IIA with ab138498 antibody at a dilution of 1/250.

    This data was developed using the same antibody clone in a different buffer formulation containing PBS, BSA, glycerol, and sodium azide (ab138498).

  • Immunofluorescent analysis of A431 cells labelling non-muscle Myosin IIA with ab138498 at 1/250 dilution.

    This data was developed using the same antibody clone in a different buffer formulation containing PBS, BSA, glycerol, and sodium azide (ab138498).

  • Immunofluorescent analysis of HeLa cells labelling non-muscle Myosin IIA with ab138498 at 1/250 dilution.

    This data was developed using the same antibody clone in a different buffer formulation containing PBS, BSA, glycerol, and sodium azide (ab138498).

References

ab236073 has not yet been referenced specifically in any publications.

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