ArticleFrontiers in cellular neuroscience2015
TMEM16A is associated with voltage-gated calcium channels in mouse retina and its function is disrupted upon mutation of the auxiliary α2δ4 subunit.
Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- Dysfunction of α2δ4 leads to photoreceptor degeneration through disrupted synaptic mitochondria and calcium crosstalk.Cell death & disease · 2026Article
- Analysis of the relationship between rod cell membrane currents and the photoreceptor component of electroretinograms using a cable model.Scientific reports · 2025Article
- Depleted Calcium Stores and Increased Calcium Entry in Rod Photoreceptors of theInternational journal of molecular sciences · 2022Article
- Role of ANO1 in tumors and tumor immunity.Journal of cancer research and clinical oncology · 2022Review
- Reduced Expression of TMEM16A Impairs Nitric Oxide-Dependent ClFrontiers in cellular neuroscience · 2022Article
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- Development and maintenance of vision's first synapse.Developmental biology · 2021Review
- A paradoxical increase of force development in saphenous and tail arteries from heterozygous ANO1 knockout mice.Physiological reports · 2020Article
- Bayesian inference for biophysical neuron models enables stimulus optimization for retinal neuroprosthetics.eLife · 2020Article
- Sensing through Non-Sensing Ocular Ion Channels.International journal of molecular sciences · 2020Review
- Emerging roles for α2δ subunits in calcium channel function and synaptic connectivity.Current opinion in neurobiology · 2020Review
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- Hydroxyindole-Heliyon · 2019Article
- Voltage- and calcium-gated ion channels of neurons in the vertebrate retina.Progress in retinal and eye research · 2019Review
- αThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Endoplasmic reticulum (ER) CaThe Journal of biological chemistry · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Photoreceptors rely upon highly specialized synapses to efficiently transmit signals to multiple postsynaptic targets. Calcium influx in the presynaptic terminal is mediated by voltage-gated calcium channels (VGCC). This event triggers neurotransmitter release, but also gates calcium-activated chloride channels (TMEM), which in turn regulate VGCC activity. In order to investigate the relationship between VGCC and TMEM channels, we analyzed the retina of wild type (WT) and Cacna2d4 mutant mice, in which the VGCC auxiliary α2δ4 subunit carries a nonsense mutation, disrupting the normal channel function. Synaptic terminals of mutant photoreceptors are disarranged and synaptic proteins as well as TMEM16A channels lose their characteristic localization. In parallel, calcium-activated chloride currents are impaired in rods, despite unaltered TMEM16A protein levels. Co-immunoprecipitation revealed the interaction between VGCC and TMEM16A channels in the retina. Heterologous expression of these channels in tsA-201 cells showed that TMEM16A associates with the CaV1.4 subunit, and the association persists upon expression of the mutant α2δ4 subunit. Collectively, our experiments show association between TMEM16A and the α1 subunit of VGCC. Close proximity of these channels allows optimal function of the photoreceptor synaptic terminal under physiological conditions, but also makes TMEM16A channels susceptible to changes occurring to calcium channels.
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