ANO10 Membrane Protein Introduction

Introduction of ANO10

ANO10, also known as Anoctamin-10 or Transmembrane member 16K (TMEM16K), is a protein that, in humans, is encoded by the ANO10 gene. TMEM16K (ANO10) belongs to a family of ion channels and phospholipid scramblases. Mutations in ANO10 cause neurological and immunological defects, and abrogated ion transport.

Basic Information of ANO10
Protein Name	Anoctamin-10
Gene Name	ANO10
Aliases	TMEM16K
Organism	Homo sapiens (Human)
UniProt ID	Q9NW15
Transmembrane Times	8
Length (aa)	660
Sequence	MKVTLSALDTSESSFTPLVVIELAQDVKEETKEWLKNRIIAKKKDGGAQLLFRPLLNKYEQETLENQNLYLVGASKIRMLLGAEAVGLVKECNDNTMRAFTYRTRQNFKGFDDNNDDFLTMAECQFIIKHELENLRAKDEKMIPGYPQAKLYPGKSLLRRLLTSGIVIQVFPLHDSEALKKLEDTWYTRFALKYQPIDSIRGYFGETIALYFGFLEYFTFALIPMAVIGLPYYLFVWEDYDKYVIFASFNLIWSTVILELWKRGCANMTYRWGTLLMKRKFEEPRPGFHGVLGINSITGKEEPLYPSYKRQLRIYLVSLPFVCLCLYFSLYVMMIYFDMEVWALGLHENSGSEWTSVLLYVPSIIYAIVIEIMNRLYRYAAEFLTSWENHRLESAYQNHLILKVLVFNFLNCFASLFYIAFVLKDMKLLRQSLATLLITSQILNQIMESFLPYWLQRKHGVRVKRKVQALKADIDATLYEQVILEKEMGTYLGTFDDYLELFLQFGYVSLFSCVYPLAAAFAVLNNFTEVNSDALKMCRVFKRPFSEPSANIGVWQLAFETMSVISVVTNCALIGMSPQVNAVFPESKADLILIVVAVEHALLALKFILAFAIPDKPRHIQMKLARLEFESLEALKQQQMKLVTENLKEEPMESGKEKAT

Function of ANO10 Membrane Protein

ANO10, the full name which is Anoctamin-10, does not exhibit calcium-activated chloride channel (CaCC) activity but can inhibit the activity of ANO1. Belonging to a family of ion channels and phospholipid scramblases, ANO10 mutants can cause neurological and immunological defects, and abrogated ion transport. ANO10 supports migration of macrophages and phagocytosis of spirochetes. The detection of mutations in ANO10 in patients indicates that ANO10 defects cause secondary low CoQ10 and SCAR10 patients may benefit from CoQ10 supplementation.

Fig.1 Schematic representation of ANO10. (Balreira, 2014)

Application of ANO10 Membrane Protein in Literature

Wanitchakool P., et al. Cellular defects by deletion of ANO10 are due to deregulated local calcium signaling. Cell Signal. 2017, 30:41-49. PubMed ID: 27838374

This article proposes that mutations in ANO10 cause cellular defects and genetic disorders through deranged local Ca²⁺ signaling.
Chamard L., et al. Executive and Attentional Disorders, Epilepsy and Porencephalic Cyst in Autosomal Recessive Cerebellar Ataxia Type 3 Due to ANO10 Mutation. Eur Neurol. 2016, 75(3-4):186-90. PubMed ID: 27045840

This article suggests that executive and attentional disorders are impaired in ANO10 mutation. In addition, epilepsy and porencephalic cysts are also described in our ARCA3 patients, the cyst thus expanding the clinical phenotype of ARCA3 patients due to ANO10 mutation.
Hammer C., et al. A Coding Variant of ANO10, Affecting Volume Regulation of Macrophages, Is Associated with Borrelia Seropositivity. Mol Med. 2015, 21:26-37. PubMed ID: 25730773

This study demonstrates for the first time that ANO10 has a central role in innate immune defense against Borrelia infection.
Balreira A., et al. ANO10 mutations cause ataxia and coenzyme Q₁₀ deficiency. J Neurol. 2014, 261(11):2192-8. PubMed ID: 25182700

In this article, the detection of mutations in ANO10 in the patients indicate that ANO10 defects cause secondary low CoQ10 and SCAR10 patients may benefit from CoQ10 supplementation.
Maruyama H., et al. Exome sequencing reveals a novel ANO10 mutation in a Japanese patient with autosomal recessive spinocerebellar ataxia. Clin Genet. 2014. Mar;85(3):296-7. PubMed ID: 23551081

This article shows that the mutation in ANO10 can cause autosomal recessive spinocerebellar ataxia.

ANO10 Preparation Options

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Reference

Balreira A, et.al. (2014). ANO10 mutations cause ataxia and coenzyme Q₁₀ deficiency. J Neurol. Nov;261(11):2192-8.

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