ArticleAmerican journal of physiology. Heart and circulatory physiology2011
TMEM16A channels generate Ca²⁺-activated Cl⁻ currents in cerebral artery smooth muscle cells.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.
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Who cites it
81 citing papers in PubMed, 108 citations in OpenAlex.
- Loss of Vascular TMEM16A Impairs Cerebral Autoregulation and Exacerbates Ischemia-reperfusion Injury.Translational stroke research · 2026Article
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- TMEM16A channel signalling microdomains in the regulation of vascular function.The Journal of physiology · 2026Review
- Uncovering the prognostic implications and immunological roles of transmembrane protein 208 in bladder cancer by multi omics analysis and experimental verification.Scientific reports · 2025Article
- TMEM16A in gastrointestinal and vascular smooth muscle contractility.The Journal of physiology · 2025Review
- Pericyte Electrical Signalling and Brain Haemodynamics.Basic & clinical pharmacology & toxicology · 2025Review
- Acidosis enhances contribution of CaCurrent research in physiology · 2025Article
- TMEM16 proteins: CaInternational journal of molecular medicine · 2024Review
- TMEM44 as a Novel Prognostic Marker for Kidney Renal Clear Cell Carcinoma is Associated with Tumor Invasion, Migration and Immune Infiltration.Biochemical genetics · 2024Article
- Extracellular glucose and dysfunctional insulin receptor signaling independently upregulate arterial smooth muscle TMEM16A expression.American journal of physiology. Cell physiology · 2024Article
- Transmembrane protein 176B regulates amino acid metabolism through the PI3K-Akt-mTOR signaling pathway and promotes gastric cancer progression.Cancer cell international · 2024Article
- Expression of TMEM59L associated with radiosensitive in glioblastoma.Journal of radiation research · 2023Article
- Rare variants in ANO1, encoding a calcium-activated chloride channel, predispose to moyamoya disease.Brain : a journal of neurology · 2023Article
- Mechanical stimulation controls osteoclast function through the regulation of CaCommunications biology · 2023Article
- Interspecies and regional variability of alcohol action on large cerebral arteries: regulation by KCNMB1 proteins.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Article
- Vascular mechanotransduction.Physiological reviews · 2023Review
- Locus specific endogenous retroviral expression associated with Alzheimer's disease.Frontiers in aging neuroscience · 2023Article
- Polymodal Control of TMEM16x Channels and Scramblases.International journal of molecular sciences · 2022Review
- TMEM158 Regulates the Canonical and Non-Canonical Pathways of TGF-β to Mediate EMT in Triple-Negative Breast Cancer.Journal of Cancer · 2022Article
- TMEM16A Plays an Insignificant Role in Myocardium Remodeling but May Promote Angiogenesis of Heart During Pressure-overload.Frontiers in physiology · 2022Article
21 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Transmembrane protein (TMEM)16A channels are recently discovered membrane proteins that display electrophysiological properties similar to classic Ca(2+)-activated Cl(-) (Cl(Ca)) channels in native cells. The molecular identity of proteins that generate Cl(Ca) currents in smooth muscle cells (SMCs) of resistance-size arteries is unclear. Similarly, whether cerebral artery SMCs generate Cl(Ca) currents is controversial. Here, using molecular biology and patch-clamp electrophysiology, we examined TMEM16A channel expression and characterized Cl(-) currents in arterial SMCs of resistance-size rat cerebral arteries. RT-PCR amplified transcripts for TMEM16A but not TMEM16B-TMEM16H, TMEM16J, or TMEM16K family members in isolated pure cerebral artery SMCs. Western blot analysis using an antibody that recognized recombinant (r)TMEM16A channels detected TMEM16A protein in cerebral artery lysates. Arterial surface biotinylation and immunofluorescence indicated that TMEM16A channels are located primarily within the arterial SMC plasma membrane. Whole cell Cl(Ca) currents in arterial SMCs displayed properties similar to those generated by rTMEM16A channels, including Ca(2+) dependence, current-voltage relationship linearization by an elevation in intracellular Ca(2+) concentration, a Nerstian shift in reversal potential induced by reducing the extracellular Cl(-) concentration, and a negative reversal potential shift when substituting extracellular I(-) for Cl(-). A pore-targeting TMEM16A antibody similarly inhibited both arterial SMC Cl(Ca) and rTMEM16A currents. TMEM16A knockdown using small interfering RNA also inhibited arterial SMC Cl(Ca) currents. In summary, these data indicate that TMEM16A channels are expressed, insert into the plasma membrane, and generate Cl(Ca) currents in cerebral artery SMCs.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.