ArticleCell death & disease2013
Calcium-activated and apoptotic phospholipid scrambling induced by Ano6 can occur independently of Ano6 ion currents.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Evaluation of translational potential of mRNA vaccine candidate antigens for pancreatic cancer: a systematic review based on clinical evidence and stratified prioritization strategies.Frontiers in immunology · 2026Pooled it
- Scott syndrome with novel compound heterozygous pathogenic variants in ANO6 and reduced thrombin generation.Haematologica · 2026Article
- High glucose enhances NScientific reports · 2026Article
- Role of Rubicon in platelets: a promoter of thrombosis but not an autophagy repressor.Blood advances · 2026Article
- Simulation-based survey of TMEM16 family reveals that robust lipid scrambling requires an open groove.eLife · 2025Article
- Simulation-based survey of TMEM16 family reveals that robust lipid scrambling requires an open groove.bioRxiv : the preprint server for biology · 2025Article
- TMEM16E regulates endothelial cell procoagulant activity and thrombosis.The Journal of clinical investigation · 2023Article
- Trpc6 gain-of-function disease mutation enhances phosphatidylserine exposure in murine platelets.PloS one · 2022Article
- Establishment of a novel CNV-related prognostic signature predicting prognosis in patients with breast cancer.Journal of ovarian research · 2021Article
- Article
- Plasma membrane-localized TMEM16 proteins are indispensable for expression of CFTR.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Temperature-dependent increase in the calcium sensitivity and acceleration of activation of ANO6 chloride channel variants.Scientific reports · 2019Article
- Article
- ATP-Gated P2X7 Receptors Require Chloride Channels To Promote Inflammation in Human Macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Oxidative stress, autophagy and airway ion transport.American journal of physiology. Cell physiology · 2019Review
- ANO6 promotes cell proliferation and invasion in glioma through regulating the ERK signaling pathway.OncoTargets and therapy · 2019Article
- Known structures and unknown mechanisms of TMEM16 scramblases and channels.The Journal of general physiology · 2018Review
- Regulation and Function of TMEM16F in Renal Podocytes.International journal of molecular sciences · 2018Article
- Contribution of TMEM16F to pyroptotic cell death.Cell death & disease · 2018Article
- Regulation of TMEM16A/ANO1 and TMEM16F/ANO6 ion currents and phospholipid scrambling by CaThe Journal of physiology · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune cells and platelets maintain plasma membrane phospholipid asymmetry. Upon activation, this asymmetry is disrupted by phospholipid scrambling (PS), which is a major step during activation of immune cells, hemostasis and apoptosis. Anoctamin 6 (Ano6; TMEM16F) causes chloride (Cl(-)) and cation currents and is required for Ca(2+)-dependent PS. It is defective in blood cells from patients with Scott syndrome, a rare bleeding disorder. We examined if Cl(-) currents and PS are related, whether both processes are Ca(2+) dependent, and whether Ca(2+)-independent scrambling during intrinsic and extrinsic apoptosis is controlled by Ano6. Ca(2+) increase by ionomycin activated Ano6 Cl(-) currents and PS in normal lymphocytes, but not in B-lymphocytes from two different patients with Scott syndrome. Fas ligand (FasL) did not increase intracellular Ca(2+), but activated Cl(-) currents in normal but not in Scott lymphocytes. Whole-cell currents were inhibited by Cl(-) channel blockers and by siRNA knockdown of Ano6. In contrast, intrinsic mitochondrial apoptosis by ABT-737 did not induce Cl(-) currents in lymphocytes. PS was not inhibited by blockers of Ano6 or removal of Cl(-) ions. Remarkably, Ca(2+)-independent scrambling due to extrinsic (FasL) or intrinsic (ABT-737) apoptosis was unchanged in Scott cells. We conclude that: (i) Ano6 Cl(-) currents are activated by increase in cytosolic Ca(2+), or Ca(2+) independent by stimulation of Fas receptors; (ii) Ca(2+)-dependent PS induced by Ano6 does not require Cl(-) currents; (iii) Ca(2+)-independent PS does not require Ano6; (iv) Ano6 is necessary for Ca(2+)-dependent PS, but not by increasing intracellular Ca(2+).
Indexed as
Identifiers
What OpenQuestion holds
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.