ReviewJournal of molecular biology2015
TMEM16 proteins: unknown structure and confusing functions.
Review in Journal of molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
82 citing papers in PubMed, 137 citations in OpenAlex.
- Trial
- Anoctamin 5 as a protective factor in prostate cancer: Insights from WGCNA, machine learning, and experimental analysis, with a focus on the anoctamin family.Translational oncology · 2026Article
- Pan-Cancer Analysis of ANO6 and Experimental Validation in Metastatic Melanoma.Biochemical genetics · 2026Article
- Multiple roles of ANO6 in tumors, molecular mechanism and its potential therapeutic value.Biochemistry and biophysics reports · 2025Review
- Genomic scans for selection and runs of homozygosity in southern Italian turkey populations.Poultry science · 2025Article
- Transcriptomic profiling of backfat and muscle in Lijiang pigs with divergent body size across growth stages.Scientific reports · 2024Article
- The ion channel Anoctamin 10/TMEM16K coordinates organ morphogenesis across scales in the urochordate notochord.PLoS biology · 2024Article
- Determining expression changes of ANO7 and SLC38A4 membrane transporters in colorectal cancer.Heliyon · 2024Article
- Missense variants in ANO4 cause sporadic encephalopathic or familial epilepsy with evidence for a dominant-negative effect.American journal of human genetics · 2024Article
- Sperm epigenetics and male infertility: unraveling the molecular puzzle.Human genomics · 2024Review
- Transmembrane proteins with unknown function (TMEMs) as ion channels: electrophysiological properties, structure, and pathophysiological roles.Experimental & molecular medicine · 2024Review
- Article
- Anoctamins and Calcium Signalling: An Obstacle to EGFR Targeted Therapy in Glioblastoma?Cancers · 2022Review
- Activation of TMEM16F by inner gate charged mutations and possible lipid/ion permeation mechanisms.Biophysical journal · 2022Article
- CaInternational journal of molecular sciences · 2022Article
- Polymodal Control of TMEM16x Channels and Scramblases.International journal of molecular sciences · 2022Review
- ATP Synthase KFunction (Oxford, England) · 2022Article
- Anion and Cation Permeability of the Mouse TMEM16F Calcium-Activated Channel.International journal of molecular sciences · 2021Article
- The ATP-Releasing Maxi-Cl Channel: Its Identity, Molecular Partners and Physiological/Pathophysiological Implications.Life (Basel, Switzerland) · 2021Review
- Annexins and Membrane Repair Dysfunctions in Muscular Dystrophies.International journal of molecular sciences · 2021Review
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The TMEM16 family of membrane proteins, also known as anoctamins, plays key roles in a variety of physiological functions that range from ion transport to phospholipid scrambling and to regulating other ion channels. The first two family members to be functionally characterized, TMEM16A (ANO1) and TMEM16B (ANO2), form Ca(2+)-activated Cl(-) channels and are important for transepithelial ion transport, olfaction, phototransduction, smooth muscle contraction, nociception, cell proliferation and control of neuronal excitability. The roles of other family members, such as TMEM16C (ANO3), TMEM16D (ANO4), TMEM16F (ANO6), TMEM16G (ANO7) and TMEM16J (ANO9), remain poorly understood and controversial. These homologues were reported to be phospholipid scramblases, ion channels, to have both functions or to be regulatory subunits of other channels. Mutations in TMEM16F cause Scott syndrome, a bleeding disorder caused by impaired Ca(2+)-dependent externalization of phosphatidylserine in activated platelets, suggesting that this homologue might be a scramblase. However, overexpression of TMEM16F has also been associated with a remarkable number of different ion channel types, raising the possibility that this protein might be involved in both ion and lipid transports. The recent identification of an ancestral TMEM16 homologue with intrinsic channel and scramblase activities supports this hypothesis. Thus, the TMEM16 family might have diverged in two or three different subclasses, channels, scramblases and dual-function channel/scramblases. The structural bases and functional implication of such a functional diversity within a single protein family remain to be elucidated and the links between TMEM16 functions and human physiology and pathologies need to be investigated.
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Registered trials
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.