ANO5, Blocking Peptide

Anoctamin-5; Gnathodiaphyseal dysplasia 1 protein; Transmembrane protein 16E; ANO5; GDD1; TMEM16E

For Research Use Only. Not for use in diagnostic procedures.

The synthetic peptide sequence used to generate the antibody was selected from the C-term region of human ANO5. A 10 to 100 fold molar excess to antibody is recommended. Precise conditions should be optimized for a particular assay.

Synthetic peptide was lyophilized with 100% acetonitrile and is supplied as a powder.

Maintain refrigerated at 2-8 degree C for up to 6 months. For long term storage store at -20 degree C.

Small volumes of ANO5 blocking peptide vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Does not exhibit calcium-activated chloride channel (CaCC) activity.

107,188 Da

anoctamin 5

anoctamin-5

Anoctamin-5

GDD1; TMEM16E  [Similar Products]

This gene encodes a member of the anoctamin family of transmembrane proteins. The encoded protein is likely a calcium activated chloride channel. Mutations in this gene have been associated with gnathodiaphyseal dysplasia. Alternatively spliced transcript variants have been described. [provided by RefSeq, Nov 2009]

ANO5: May act as a calcium-activated chloride channel. Defects in ANO5 are the cause of gnathodiaphyseal dysplasia (GDD); 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). 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). 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. Belongs to the anoctamin family.

Protein type: Channel, chloride; Membrane protein, integral; Membrane protein, multi-pass; Transporter; Transporter, ion channel

Chromosomal Location of Human Ortholog: 11p14.3

Cellular Component: intracellular; plasma membrane

Molecular Function: intracellular calcium activated chloride channel activity

Biological Process: chloride transport

Disease: Gnathodiaphyseal Dysplasia; Miyoshi Muscular Dystrophy 3; Muscular Dystrophy, Limb-girdle, Type 2l

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