ArticleEMBO reports2009
Intracellular regulation of human ClC-5 by adenine nucleotides.
Article in EMBO reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 53 citations in OpenAlex.
- The secreted protein PCYOX1L controls the surface expression of acid-sensing ion channel 1a.Science advances · 2025Article
- Structural basis of adenine nucleotides regulation and neurodegenerative pathology in ClC-3 exchanger.Nature communications · 2024Article
- Characterization of pre-mRNA Splicing Defects Caused byBiomedicines · 2023Article
- Molecular basis of ClC-6 function and its impairment in human disease.Science advances · 2023Article
- Molecular mechanism underlying regulation of Arabidopsis CLCa transporter by nucleotides and phospholipids.Nature communications · 2023Article
- Biophysical Aspects of Neurodegenerative and Neurodevelopmental Disorders Involving Endo-/Lysosomal CLC ClLife (Basel, Switzerland) · 2023Review
- Review
- Metabolic energy sensing by mammalian CLC anion/proton exchangers.EMBO reports · 2020Article
- ClThe Journal of biological chemistry · 2020Article
- Genetic Analyses in Dent Disease and Characterization of CLCN5 Mutations in Kidney Biopsies.International journal of molecular sciences · 2020Article
- Making a Dent in Dent Disease.Function (Oxford, England) · 2020Review
- Role of CBS and Bateman Domains in Phosphorylation-Dependent Regulation of a CLC Anion Channel.Biophysical journal · 2016Article
- Functional and transport analyses of CLCN5 genetic changes identified in Dent disease patients.Physiological reports · 2016Article
- Crystal Structures of the Extracellular Domain from PepT1 and PepT2 Provide Novel Insights into Mammalian Peptide Transport.Structure (London, England : 1993) · 2015Article
- A tale of two CLCs: biophysical insights toward understanding ClC-5 and ClC-7 function in endosomes and lysosomes.The Journal of physiology · 2015Review
- Structure and gating of CLC channels and exchangers.The Journal of physiology · 2015Review
- Conformational changes required for H(+)/Cl(-) exchange mediated by a CLC transporter.Nature structural & molecular biology · 2014Article
- Regulation of ClC-2 gating by intracellular ATP.Pflugers Archiv : European journal of physiology · 2013Article
- Functional characterization of a ClC transporter by solid-supported membrane electrophysiology.The Journal of general physiology · 2013Article
- Ion channels in renal disease.Chemical reviews · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
ClC-5, an endosomal Cl(-)/H(+) antiporter that is mutated in Dent disease, is essential for endosomal acidification and re-uptake of small molecular weight proteins in the renal proximal tubule. Eukaryotic chloride channels (CLCs) contain two cytoplasmic CBS domains, motifs present in different proteins, the function of which is still poorly understood. Structural studies have shown that ClC-5 can bind to ATP at the interface between the CBS domains, but so far the potential functional consequences of nucleotide binding to ClC-5 have not been investigated. Here, we show that the direct application of ATP, ADP and AMP in inside-out patch experiments potentiates the current mediated by ClC-5 with similar affinities. The nucleotides increase the probability of ClC-5 to be in an active, transporting state. The residues Tyr 617 and Asp 727, but not Ser 618, are crucial for the potentiation. These results provide a mechanistic and structural framework for the interpretation of nucleotide regulation of a CLC transporter.
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.