ArticleThe Journal of biological chemistry2015
Anoctamin-6 controls bone mineralization by activating the calcium transporter NCX1.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses 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
30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.
- Transethnic Evaluation Identifies Low-Frequency Loci Associated With 25-Hydroxyvitamin D Concentrations.The Journal of clinical endocrinology and metabolism · 2018Pooled it
- Life-Course Genome-wide Association Study Meta-analysis of Total Body BMD and Assessment of Age-Specific Effects.American journal of human genetics · 2018Pooled it
- High glucose enhances NScientific reports · 2026Article
- Calcium dependent activation of the TMEM16F scramblase and ion channel.Nature structural & molecular biology · 2026Article
- TMEM63 proteins act as mechanically activated cholesterol modulated lipid scramblases contributing to membrane mechano-resilience.Nature communications · 2026Article
- An In Vivo Model of Estrogen Supplementation Concerning the Expression of CaJournal of cardiovascular development and disease · 2024Article
- TMEM16F Expressed in Kupffer Cells Regulates Liver Inflammation and Metabolism to Protect Against Listeria Monocytogenes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Functional Interdependence of Anoctamins May Influence Conclusions from Overexpression Studies.International journal of molecular sciences · 2024Article
- The ion channel Anoctamin 10/TMEM16K coordinates organ morphogenesis across scales in the urochordate notochord.PLoS biology · 2024Article
- TMEM16F scramblase regulates angiogenesis via endothelial intracellular signaling.Journal of cell science · 2024Article
- TMEM16F exacerbates tau pathology and mediates phosphatidylserine exposure in phospho-tau-burdened neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Knockdown of best1 Gene in Zebrafish Caused Abnormal Neuronal and Skeletal Development - A Subtype of Craniovertebral Junction Malformation?Neurospine · 2024Article
- Structural heterogeneity of the ion and lipid channel TMEM16F.Nature communications · 2024Article
- Integration of metabolomics and transcriptomics provides insights into enhanced osteogenesis inFrontiers in endocrinology · 2023Article
- First genome-wide association study of 99 body measures derived from 3-dimensional body scans.Genes & diseases · 2022Article
- Electrophysiological Properties of Endogenous Single CaInternational journal of molecular sciences · 2021Article
- Molecular underpinning of intracellular pH regulation on TMEM16F.The Journal of general physiology · 2021Article
- Critical Role of Lipid Scramblase TMEM16F in Phosphatidylserine Exposure and Repair of Plasma Membrane after Pore Formation.Cell reports · 2020Article
- Cryo-EM Studies of TMEM16F Calcium-Activated Ion Channel Suggest Features Important for Lipid Scrambling.Cell reports · 2019Article
- Plasma membrane-localized TMEM16 proteins are indispensable for expression of CFTR.Journal of molecular medicine (Berlin, Germany) · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Anoctamin-6 (Ano6, TMEM16F) belongs to a family of putative Ca(2+)-activated Cl(-) channels and operates as membrane phospholipid scramblase. Deletion of Ano6 leads to reduced skeleton size, skeletal deformities, and mineralization defects in mice. However, it remains entirely unclear how a lack of Ano6 leads to a delay in bone mineralization by osteoblasts. The Na(+)/Ca(2+) exchanger NCX1 was found to interact with Ano6 in a two-hybrid split-ubiquitin screen. Using human osteoblasts and osteoblasts from Ano6(-/-) and WT mice, we demonstrate that NCX1 requires Ano6 to efficiently translocate Ca(2+) out of osteoblasts into the calcifying bone matrix. Ca(2+)-activated anion currents are missing in primary osteoblasts isolated from Ano6 null mice. Our findings demonstrate the importance of NCX1 for bone mineralization and explain why deletion of an ion channel leads to the observed mineralization defect: Ano6 Cl(-) currents are probably required to operate as a Cl(-) bypass channel, thereby compensating net Na(+) charge movement by NCX1.
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.