Key features and details
- Rabbit polyclonal to anoctamin 5
- Suitable for: WB, IHC-P, ELISA
- Reacts with: Human
- Isotype: IgG
Product nameAnti-anoctamin 5 antibody
DescriptionRabbit polyclonal to anoctamin 5
Tested applicationsSuitable for: WB, IHC-P, ELISAmore details
Species reactivityReacts with: Human
Predicted to work with: Mouse
Synthetic peptide within Human anoctamin 5 (N terminal). The exact sequence is proprietary.
Database link: Q75V66
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In preparation for this, we have started to update the applications & species that this product is Abpromise guaranteed for.
We are also updating the applications & species that this product has been “predicted to work with,” however this information is not covered by our Abpromise guarantee.
Applications & species from publications and Abreviews that have not been tested in our own labs or in those of our suppliers are not covered by the Abpromise guarantee.
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Storage instructionsShipped 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.
Concentration information loading...
Our Abpromise guarantee covers the use of ab181663 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||1/500 - 1/2000. Predicted molecular weight: 107 kDa.|
|IHC-P||1/50 - 1/500.|
|ELISA||Use at an assay dependent concentration.|
FunctionMay act as a calcium-activated chloride channel.
Tissue specificityHighly expressed in brain, heart, kidney, lung, and skeletal muscle. Weakly expressed in bone marrow, fetal liver, placenta, spleen, thymus, osteoblasts and periodontal ligament cells.
Involvement in diseaseDefects in ANO5 are the cause of gnathodiaphyseal dysplasia (GDD) [MIM:166260]; also known as osteogenesis imperfecta with unusual skeletal lesions or gnathodiaphyseal sclerosis. GDD is a rare skeletal syndrome characterized by bone fragility, sclerosis of tubular bones, and cemento-osseous lesions of the jawbone. Patients experience frequent bone fractures caused by trivial accidents in childhood; however the fractures heal normally without bone deformity. The jaw lesions replace the tooth-bearing segments of the maxilla and mandible with fibrous connective tissues, including various amounts of cementum-like calcified mass, sometimes causing facial deformities. Patients also have a propensity for jaw infection and often suffer from purulent osteomyelitis-like symptoms, such as swelling of and pus discharge from the gums, mobility of the teeth, insufficient healing after tooth extraction and exposure of the lesions into the oral cavity.
Defects in ANO5 are the cause of limb-girdle muscular dystrophy type 2L (LGMD2L) [MIM:611307]. It is an autosomal recessive degenerative myopathy characterized by proximal weakness, weakness of the hip and shoulder girdles and prominent asymmetrical quadriceps femoris and biceps brachii atrophy.
Defects in ANO5 are the cause of miyoshi muscular dystrophy type 3 (MMD3) [MIM:613319]. It is a late-onset muscular dystrophy characterized by distal muscle weakness of the lower limbs, calf muscle discomfort and weakness, quadriceps atrophy. Muscle weakness and atrophy may be asymmetric.
Sequence similaritiesBelongs to the anoctamin family.
Cellular localizationEndoplasmic reticulum membrane. Co-localized with CALR/calreticulin.
- Information by UniProt
- Ano5 antibody
- ANO5_HUMAN antibody
- Anoctamin-5 antibody
ab181663 has been referenced in 1 publication.
- Song HY et al. Anoctamin 5 regulates cell proliferation and migration in pancreatic cancer. Int J Clin Exp Pathol 12:4263-4270 (2019). PubMed: 31933826