ReviewAmerican journal of physiology. Renal physiology2016
New perspective of ClC-Kb/2 Cl- channel physiology in the distal renal tubule.
Review in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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
19 citing papers in PubMed, 30 citations in OpenAlex.
- Integrated transcriptomic and single-cell RNA-seq analysis identifies CLCNKB, KLK1 and PLEKHA4 as key gene of AKI-to-CKD progression.Frontiers in immunology · 2025Article
- ClC-Kb pore mutation disrupts glycosylation and triggers distal tubular remodeling.JCI insight · 2024Article
- Genomic adaptation to small population size and saltwater consumption in the critically endangered Cat Ba langur.Nature communications · 2024Article
- Sex differences in renal transporters: assessment and functional consequences.Nature reviews. Nephrology · 2024Review
- Persistent mild hypokalemia in an otherwise healthy 6-year-old girl: Answers.Pediatric nephrology (Berlin, Germany) · 2022Article
- ClC-K2 ClFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Dietary potassium and the kidney: lifesaving physiology.Clinical kidney journal · 2020Review
- Multiple acid-base and electrolyte disturbances upregulate NBCn1, NBCn2, IRBIT and L-IRBIT in the mTAL.The Journal of physiology · 2020Article
- Vibrodissociation method for isolation of defined nephron segments from human and rodent kidneys.American journal of physiology. Renal physiology · 2019Article
- Clinical importance of potassium intake and molecular mechanism of potassium regulation.Clinical and experimental nephrology · 2019Review
- Intracellular chloride: a regulator of transepithelial transport in the distal nephron.Current opinion in nephrology and hypertension · 2019Review
- Renal Tubular Acidosis: HAdvances in chronic kidney disease · 2018Review
- A selective class of inhibitors for the CLC-Ka chloride ion channel.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Role of ClC-K and barttin in low potassium-induced sodium chloride cotransporter activation and hypertension in mouse kidney.Bioscience reports · 2018Article
- Dietary KPflugers Archiv : European journal of physiology · 2018Article
- PGFAmerican journal of physiology. Renal physiology · 2017Article
- WNK Kinases in Development and Disease.Current topics in developmental biology · 2017Review
- Role and mechanisms of regulation of the basolateral KActa physiologica (Oxford, England) · 2017Review
- Alkaline activation of ClC-K2 chloride channels switches renal cells from reabsorbing to secreting.The Journal of general physiology · 2016Article
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 at 2 institutions in 1 country.
Funding
Abstract
Since its identification as the underlying molecular cause of Bartter's syndrome type 3, ClC-Kb (ClC-K2 in rodents, henceforth it will be referred as ClC-Kb/2) is proposed to play an important role in systemic electrolyte balance and blood pressure regulation by controlling basolateral Cl(-) exit in the distal renal tubular segments from the cortical thick ascending limb to the outer medullary collecting duct. Considerable experimental and clinical effort has been devoted to the identification and characterization of disease-causing mutations as well as control of the channel by its cofactor, barttin. However, we have only begun to unravel the role of ClC-Kb/2 in different tubular segments and to reveal the regulators of its expression and function, e.g., insulin and IGF-1. In this review we discuss recent experimental evidence in this regard and highlight unexplored questions critical to understanding ClC-Kb/2 physiology in the kidney.
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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.