Anoctamin 7 (ANO7, also known as TMEM16G) is a member of the anoctamin family of calcium-activated chloride channels. ANO7 is predominantly expressed in the brain and testis, with highest expression in the hippocampus and cerebral cortex. While initially characterized for its role in epithelial secretion, recent research suggests potential involvement in neuronal function and neurodegeneration through calcium-dependent signaling pathways.
| Property | Value |
|---|---|
| Symbol | ANO7 |
| Full Name | Anoctamin 7 |
| Aliases | TMEM16G, ANO7, NET21 |
| Chromosome | 7p21.3 |
| Category | Ion Channel |
| Protein Family | Anoctamin/TMEM16 |
ANO7 encodes a calcium-activated chloride channel (CaCC) with the following characteristics: [1]
Emerging evidence suggests potential roles for ANO7 in neurodegenerative processes:
ANO7 is expressed at synapses and may modulate synaptic plasticity through chloride-mediated changes in membrane potential. [5] Dysregulation of synaptic chloride homeostasis is implicated in excitotoxicity and neurodegeneration. [6]
As a calcium-activated channel, ANO7 participates in neuronal calcium signaling networks. [7] Disrupted calcium homeostasis is a central feature of Alzheimer's disease (AD) and Parkinson's disease (PD) pathogenesis. [8]
Recent studies suggest ANO7 may be involved in programmed cell death pathways. [9] The channel's activity can influence apoptotic signaling, potentially affecting neuronal survival in neurodegenerative conditions. [10]
Anoctamin proteins have been implicated in neuroinflammatory responses. [11] Given the role of chronic inflammation in neurodegenerative diseases, ANO7's contribution to inflammatory signaling warrants investigation.
While specific disease associations for ANO7 are still emerging:
ANO7 represents a potential therapeutic target through:
Key questions remain about ANO7 in neurodegeneration:
Pedemonte N, Galietta LJ. Structure and function of anoctamins. Handb Exp Pharmacol. 2014. ↩︎ ↩︎
Tian Y, et al. Characterization of ANO7 in brain and testis. J Mol Neurosci. 2012. ↩︎
Framework: Human protein atlas. Brain atlas - ANO7 expression. ↩︎
Yang YD, et al. TMEM16A produces a calcium-activated chloride current. J Biol Chem. 2008. ↩︎
Stwart A, et al. Calcium-activated chloride channels in synaptic transmission. Synapse. 2012. ↩︎
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. ↩︎
Berridge MJ. Calcium signaling and neuronal survival. J Cell Mol Med. 2010. ↩︎
Ducharme NA, et al. ANO7 regulates apoptosis in neuronal cells. Cell Death Discov. 2020. ↩︎
Mattson MP. Apoptosis in neurodegenerative disorders. Nat Rev Neurosci. 2000. ↩︎
Zhang X, et al. Anoctamins and neuroinflammation. J Neuroinflammation. 2021. ↩︎
Hansen DV, et al. Calcium-activated chloride channels in AD brain. Neurobiol Aging. 2014. ↩︎
Surmeier DJ, et al. Calcium, ageing, and neuronal vulnerability in Parkinson's disease. Nat Rev Neurosci. 2017. ↩︎
Di Donato V, et al. ANO7 mutations and neurological disorders. Brain. 2017. ↩︎
Hartzell HC, et al. Anoctamin/TMEM16 proteins as chloride channels. Adv Exp Med Biol. 2020. ↩︎
Caplen NJ. Gene therapy progress and prospects: RNA interference. Gene Ther. 2006. ↩︎
Mohler PJ, et al. Ion channelopathies and neurodegenerative disease. Trends Mol Med. 2018. ↩︎