ArticlePloS one2015
SLC26A Gene Family Participate in pH Regulation during Enamel Maturation.
Article in PloS one, 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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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.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Prenatal exposure to gestational diabetes mellitus increases developmental defects in the enamel of offspring.PloS one · 2019Trial
- The Role of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) in Enamel Formation.Calcified tissue international · 2026Article
- Ano1 Antisense Therapy Improves Enamel Properties in Molars but not Amelogenesis in a Murine Model of Cystic Fibrosis.Calcified tissue international · 2026Article
- Review
- SLC26 Anion Transporters.Handbook of experimental pharmacology · 2024Review
- Rare variants in the endocytic pathway are associated with Alzheimer's disease, its related phenotypes, and functional consequences.PLoS genetics · 2021Article
- SLC26A7 constitutes the thiocyanate-selective anion conductance of the basolateral membrane of the retinal pigment epithelium.American journal of physiology. Cell physiology · 2020Article
- The Fundamental Role of Bicarbonate Transporters and Associated Carbonic Anhydrase Enzymes in Maintaining Ion and pH Homeostasis in Non-Secretory Organs.International journal of molecular sciences · 2020Review
- Physiological and Pathological Functions of SLC26A6.Frontiers in medicine · 2020Review
- Physiological and Pathophysiological Relevance of the Anion Transporter Slc26a9 in Multiple Organs.Frontiers in physiology · 2018Review
- Bicarbonate Transport During Enamel Maturation.Calcified tissue international · 2017Review
- DENTAL ENAMEL FORMATION AND IMPLICATIONS FOR ORAL HEALTH AND DISEASE.Physiological reviews · 2017Review
- Enamel: Molecular identity of its transepithelial ion transport system.Cell calcium · 2017Review
- MiR-153 Regulates Amelogenesis by Targeting Endocytotic and Endosomal/lysosomal Pathways-Novel Insight into the Origins of Enamel Pathologies.Scientific reports · 2017Article
- DLX3-Dependent Regulation of Ion Transporters and Carbonic Anhydrases is Crucial for Enamel Mineralization.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017Article
- Deletion ofFrontiers in physiology · 2017Article
- The Role of Na:K:2Cl Cotransporter 1 (NKCC1/SLC12A2) in Dental Epithelium during Enamel Formation in Mice.Frontiers in physiology · 2017Article
- Multiple Calcium Export Exchangers and Pumps Are a Prominent Feature of Enamel Organ Cells.Frontiers in physiology · 2017Article
- Extracellular Cl(-) regulates human SO4 (2-)/anion exchanger SLC26A1 by altering pH sensitivity of anion transport.Pflugers Archiv : European journal of physiology · 2016Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
Abstract
The bicarbonate transport activities of Slc26a1, Slc26a6 and Slc26a7 are essential to physiological processes in multiple organs. Although mutations of Slc26a1, Slc26a6 and Slc26a7 have not been linked to any human diseases, disruption of Slc26a1, Slc26a6 or Slc26a7 expression in animals causes severe dysregulation of acid-base balance and disorder of anion homeostasis. Amelogenesis, especially the enamel formation during maturation stage, requires complex pH regulation mechanisms based on ion transport. The disruption of stage-specific ion transporters frequently results in enamel pathosis in animals. Here we present evidence that Slc26a1, Slc26a6 and Slc26a7 are highly expressed in rodent incisor ameloblasts during maturation-stage tooth development. In maturation-stage ameloblasts, Slc26a1, Slc26a6 and Slc26a7 show a similar cellular distribution as the cystic fibrosis transmembrane conductance regulator (Cftr) to the apical region of cytoplasmic membrane, and the distribution of Slc26a7 is also seen in the cytoplasmic/subapical region, presumably on the lysosomal membrane. We have also examined Slc26a1 and Slc26a7 null mice, and although no overt abnormal enamel phenotypes were observed in Slc26a1-/- or Slc26a7-/- animals, absence of Slc26a1 or Slc26a7 results in up-regulation of Cftr, Ca2, Slc4a4, Slc4a9 and Slc26a9, all of which are involved in pH homeostasis, indicating that this might be a compensatory mechanism used by ameloblasts cells in the absence of Slc26 genes. Together, our data show that Slc26a1, Slc26a6 and Slc26a7 are novel participants in the extracellular transport of bicarbonate during enamel maturation, and that their functional roles may be achieved by forming interaction units with Cftr.
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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.