ArticlePflugers Archiv : European journal of physiology2009
Functional assembly and purinergic activation of bestrophins.
Article in Pflugers Archiv : European journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Review of the clinical electrooculogram - Part 1: Mechanism of the Light-Rise.Documenta ophthalmologica. Advances in ophthalmology · 2026Review
- Evaluating BEST1 mutations in pluripotent stem cell-derived retinal pigment epithelial cells.Methods in enzymology · 2021Article
- Calcium-gated KPflugers Archiv : European journal of physiology · 2017Article
- Restoration of mutant bestrophin-1 expression, localisation and function in a polarised epithelial cell model.Disease models & mechanisms · 2016Article
- Interaction of bestrophin-1 and Ca2+ channel β-subunits: identification of new binding domains on the bestrophin-1 C-terminus.PloS one · 2011Article
- The presence of bestrophin-1 modulates the Ca2+ recruitment from Ca2+ stores in the ER.Pflugers Archiv : European journal of physiology · 2010Article
- ER-localized bestrophin 1 activates Ca2+-dependent ion channels TMEM16A and SK4 possibly by acting as a counterion channel.Pflugers Archiv : European journal of physiology · 2010Article
- Loss of TMEM16A causes a defect in epithelial Ca2+-dependent chloride transport.The Journal of biological chemistry · 2009Article
- Bestrophin 1 promotes epithelial-to-mesenchymal transition of renal collecting duct cells.Journal of the American Society of Nephrology : JASN · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proteins of the bestrophin family produce Ca(2+)-activated Cl(-) currents and regulate voltage-gated Ca(2+) channels. Bestrophin 1 was first identified in the retinal pigment epithelium. Four human paralogs (hBest1-hBest4) exist, and for some bestrophins, dimeric and heterotetrameric structures have been proposed. Here, we demonstrate that hBest1-hBest4 induce Cl(-) conductances of different amplitudes when expressed in HEK293 cells and when activated through purinergic stimulation. hBest1 mutants that are known to cause autosomal dominant macular dystrophy (Best disease) did not produce a Cl(-) current. Bestrophins were colocalized and showed molecular and functional interaction in HEK293 cells, overexpressing hBest1 and hBest2 or hBest4. Interaction was confirmed in airway epithelial cells coexpressing endogenous bestrophins. A fraction of hBest2 and hBest4 was expressed in the membrane, while most of hBest1 was found in the endoplasmic reticulum. Nevertheless, hBest1 has a clear role for the adenosine triphosphate (ATP; or uridine triphosphate)-induced Cl(-) current in both HEK293 and Calu-3 cells. Since native epithelial tissues typically express several bestrophin paralogs, these proteins may exist as heterooligomeric structures.
Indexed as
Identifiers
19130075What 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.