ArticlePflugers Archiv : European journal of physiology2010
The presence of bestrophin-1 modulates the Ca2+ recruitment from Ca2+ stores in the ER.
Article in Pflugers Archiv : European journal of physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
- TMEM16E-mediated macropinocytosis promotes cell survival under acidic stress.Cellular and molecular life sciences : CMLS · 2026Article
- CaActa physiologica (Oxford, England) · 2026Review
- Review of the clinical electrooculogram - Part 1: Mechanism of the Light-Rise.Documenta ophthalmologica. Advances in ophthalmology · 2026Review
- Review of the clinical electrooculogram - Part 2: the bestrophinopathies and modified protocols.Documenta ophthalmologica. Advances in ophthalmology · 2026Review
- Retinal response to light exposure in BEST1-mutant dogs evaluated with ultra-high resolution OCT.Vision research · 2024Article
- Endoplasmic reticulum maintains ion homeostasis required for plasma membrane repair.The Journal of cell biology · 2021Article
- Lessons learned from quantitative fundus autofluorescence.Progress in retinal and eye research · 2020Review
- Cellular Changes in Retinas From Patients WithFrontiers in cell and developmental biology · 2020Article
- A Case of Best Disease Accompanied by Pachychoroid NeovasculopathyTurkish journal of ophthalmology · 2019Article
- Multimodal Imaging in Best Vitelliform Macular Dystrophy.Investigative ophthalmology & visual science · 2019Article
- Dysregulated calcium homeostasis prevents plasma membrane repair in Anoctamin 5/TMEM16E-deficient patient muscle cells.Cell death discovery · 2019Article
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- Bestrophin 1 and retinal disease.Progress in retinal and eye research · 2017Review
- Regulation of molecular clock oscillations and phagocytic activity via muscarinic CaScientific reports · 2017Article
- Mislocalisation of BEST1 in iPSC-derived retinal pigment epithelial cells from a family with autosomal dominant vitreoretinochoroidopathy (ADVIRC).Scientific reports · 2016Article
- BESTROPHIN1 mutations cause defective chloride conductance in patient stem cell-derived RPE.Human molecular genetics · 2016Article
- A C-terminally truncated mouse Best3 splice variant targets and alters the ion balance in lysosome-endosome hybrids and the endoplasmic reticulum.Scientific reports · 2016Article
- Pharmacological Modulation of Photoreceptor Outer Segment Degradation in a Human iPS Cell Model of Inherited Macular Degeneration.Molecular therapy : the journal of the American Society of Gene Therapy · 2015Article
- Autosomal Recessive Bestrophinopathy Is Not Associated With the Loss of Bestrophin-1 Anion Channel Function in a Patient With a Novel BEST1 Mutation.Investigative ophthalmology & visual science · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bestrophin-1, mainly analyzed in overexpression experiments, functions as Ca(2+)-dependent Cl(-) channel. Analysis of endogenously expressed bestrophin-1 suggested an influence on intracellular Ca(2+). The aim of the study is to analyze the influence of endogenously expressed bestrophin-1 on Ca(2+) homeostasis. Primary cultures of retinal pigment epithelial (RPE) cells were established from wild-type and bestrophin-1-deficient mice. Intracellular free Ca(2+) ([Ca(2+)](i)) was recorded by Ca(2+) imaging; through immunocytochemistry and differential centrifugation, subcellular localization of bestrophin-1 was analyzed. RPE cells of bestrophin-1-deficient mice showed higher levels of resting [Ca(2+)](i) than cells from wild-type mice. In cells from knockout mice and wild-type mice, ATP led to increases in [Ca(2+)](i) subsequent to phospholipase C activation. ATP-induced Ca(2+) in bestrophin-1-deficient mice rose faster and decayed slower. In cells from wild-type mice, ATP led to [Ca(2+)](i) increase via depletion of Ca(2+) from thapsigargin-sensitive stores. In cells from bestrophin-1-deficient mice, ATP-dependent increase in [Ca(2+)](i) resulted in 40% of cells from depletion of bafilomycin-sensitive and in 60% from thapsigargin-sensitive Ca(2+) stores. After differential centrifugation, bestrophin-1 was found in fractions enriched of ClC-3 Cl channel and myosin-7A. Co-localization analysis of bestrophin-1, with beta-catenin or pan-cadherin, in fresh sections of porcine retina, revealed bestrophin-1 in the basolateral membrane. A portion of endogenously expressed bestrophin-1,localized in the endoplasmic reticulum, influenced uptake of Ca(2+) into Ca(2+) stores. Therefore, bestrophin-1 possibly conducts Cl(-) as counter ion for Ca(2+) uptake into cytosolic Ca(2+) stores.
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