Anoctamin 10 (ANO10, also known as TMEM16J) is a member of the anoctamin family of calcium-activated chloride channels. ANO10 is widely expressed in various tissues, including the brain, endocrine glands, and peripheral tissues. While primarily studied for its role in epithelial chloride secretion, emerging research suggests potential implications for neurodegenerative diseases through its involvement in cellular ion homeostasis and calcium signaling pathways.
| Property | Value |
|---|---|
| Symbol | ANO10 |
| Full Name | Anoctamin 10 |
| Aliases | TMEM16J, ANO10 |
| Chromosome | 3p21.31 |
| Category | Ion Channel |
| Protein Family | Anoctamin/TMEM16 |
ANO10 encodes a calcium-activated chloride channel (CaCC) that regulates chloride ion flux across cell membranes. [1] The protein is characterized by:
While direct evidence linking ANO10 to specific neurodegenerative diseases remains limited, several mechanisms suggest potential involvement:
Calcium homeostasis is critical for neuronal survival, and dysregulation contributes to neurodegenerative processes. [4] ANO10's role as a calcium-activated chloride channel positions it as a potential modulator of neuronal calcium signaling. [5]
Chloride channels help maintain neuronal membrane potential and synaptic activity. Alterations in ANO10 function could affect neuronal excitability and contribute to pathology in Alzheimer's disease (AD) and Parkinson's disease (PD). [6]
Recent studies suggest that anoctamin proteins may be involved in neuroinflammatory processes. [7] Chronic neuroinflammation is a hallmark of neurodegenerative diseases, and any contribution by ANO10 to inflammatory signaling pathways could have disease-modifying implications.
Currently, there are no ANO10-targeted therapies for neurodegenerative diseases. However, understanding ANO10 function may contribute to:
Key areas for future ANO10 research in neurodegeneration include:
Pedemonte N, Galietta LJ. Structure and function of anoctamins. Handb Exp Pharmacol. 2014. ↩︎ ↩︎
Huang F, et al. Calcium-activated chloride channels in the regulation of cell proliferation and neuronal signaling. Cold Spring Harb Perspect Biol. 2013. ↩︎
Framework: Human protein atlas. Tissue atlas - ANO10 expression. ↩︎
Berridge MJ. Calcium signaling and neuronal survival. J Cell Mol Med. 2010. ↩︎
Fallah G, et al. Anoctamin 10 is a calcium-activated chloride channel expressed in the brain. Pflugers Arch. 2011. ↩︎
Kaila K, et al. Chloride homeostasis and GABA signaling in neuronal excitability. Nat Rev Neurosci. 2014. ↩︎
Liu H, et al. Anoctamin proteins: novel calcium-activated chloride channels and beyond. Neurosci Bull. 2022. ↩︎
Hartzell HC, et al. Anoctamin/TMEM16 proteins as chloride channels. Adv Exp Med Biol. 2020. ↩︎
Mohler PJ, et al. Ion channelopathies and neurodegenerative disease. Trends Mol Med. 2018. ↩︎
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Jansen IE, et al. [Genome-wide association studies in neurodegenerative diseases](https://doi.org/10.1016/S1474-4422(19). Lancet Neurol. 2019. ↩︎
Braak H, et al. [Staging of brain pathology related to sporadic Parkinson's disease](https://doi.org/10.1016/s0197-4580(02). Neurobiol Aging. 2003. ↩︎
Aronica E, et al. Gene expression profiling in neurodegenerative diseases. Acta Neuropathol. 2015. ↩︎
Jankord R, et al. Transgenic mouse models of neurodegenerative disease. J Neurosci Res. 2017. ↩︎