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  1. Article ; Online: Novel insight on physiological regulation of the Cl

    Chambrey, Régine / Eladari, Dominique

    American journal of physiology. Renal physiology

    2023  Volume 324, Issue 5, Page(s) F431–F432

    MeSH term(s) Sulfate Transporters/genetics ; Kidney/metabolism ; Chlorides/metabolism ; Chloride-Bicarbonate Antiporters
    Chemical Substances Sulfate Transporters ; Chlorides ; Chloride-Bicarbonate Antiporters
    Language English
    Publishing date 2023-03-09
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00029.2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uc I Zs.89: Show issues Location:
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  2. Article: ClC-K Kidney Chloride Channels: From Structure to Pathology.

    Andrini, Olga / Eladari, Dominique / Picard, Nicolas

    Handbook of experimental pharmacology

    2023  Volume 283, Page(s) 35–58

    Abstract: The molecular basis of chloride transport varies all along the nephron depending on the tubular segments especially in the apical entry of the cell. The major chloride exit pathway during reabsorption is provided by two kidney-specific ClC chloride ... ...

    Abstract The molecular basis of chloride transport varies all along the nephron depending on the tubular segments especially in the apical entry of the cell. The major chloride exit pathway during reabsorption is provided by two kidney-specific ClC chloride channels ClC-Ka and ClC-Kb (encoded by CLCNKA and CLCNKB gene, respectively) corresponding to rodent ClC-K1 and ClC-K2 (encoded by Clcnk1 and Clcnk2). These channels function as dimers and their trafficking to the plasma membrane requires the ancillary protein Barttin (encoded by BSND gene). Genetic inactivating variants of the aforementioned genes lead to renal salt-losing nephropathies with or without deafness highlighting the crucial role of ClC-Ka, ClC-Kb, and Barttin in the renal and inner ear chloride handling. The purpose of this chapter is to summarize the latest knowledge on renal chloride structure peculiarity and to provide some insight on the functional expression on the segments of the nephrons and on the related pathological effects.
    MeSH term(s) Chlorides/metabolism ; Kidney ; Cell Membrane/metabolism ; Chloride Channels/genetics ; Chloride Channels/metabolism
    Chemical Substances Chlorides ; Chloride Channels
    Language English
    Publishing date 2023-02-17
    Publishing country Germany
    Document type Journal Article
    ISSN 0171-2004
    ISSN 0171-2004
    DOI 10.1007/164_2023_635
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    Sign. bis Bd. 125 (1997): 1982 A 2146: Show issues
     danach: Sign. bei den Einzelbänden: Show issues

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  3. Article ; Online: Leave NOSTONE unturned: are thiazides useless in preventing kidney stone recurrence?

    Brazier, François / Cornière, Nicolas / Eladari, Dominique

    Kidney international

    2023  Volume 104, Issue 4, Page(s) 640–643

    MeSH term(s) Humans ; Thiazides ; Kidney Calculi/prevention & control ; Nephrolithiasis ; Recurrence
    Chemical Substances Thiazides
    Language English
    Publishing date 2023-07-16
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2023.06.030
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 797: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  4. Article ; Online: Pendrin: linking acid base to blood pressure.

    Brazier, François / Cornière, Nicolas / Picard, Nicolas / Chambrey, Régine / Eladari, Dominique

    Pflugers Archiv : European journal of physiology

    2023  Volume 476, Issue 4, Page(s) 533–543

    Abstract: Pendrin (SLC26A4) is an anion exchanger from the SLC26 transporter family which is mutated in human patients affected by Pendred syndrome, an autosomal recessive disease characterized by sensoneurinal deafness and hypothyroidism. Pendrin is also ... ...

    Abstract Pendrin (SLC26A4) is an anion exchanger from the SLC26 transporter family which is mutated in human patients affected by Pendred syndrome, an autosomal recessive disease characterized by sensoneurinal deafness and hypothyroidism. Pendrin is also expressed in the kidney where it mediates the exchange of internal HCO
    MeSH term(s) Animals ; Mice ; Humans ; Blood Pressure/physiology ; Sulfate Transporters ; Kidney/metabolism ; Nephrons/metabolism ; Sodium Chloride ; Chlorides/metabolism ; Anion Transport Proteins/genetics
    Chemical Substances Sulfate Transporters ; Sodium Chloride (451W47IQ8X) ; Chlorides ; Anion Transport Proteins
    Language English
    Publishing date 2023-12-19
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 6380-0
    ISSN 1432-2013 ; 0031-6768
    ISSN (online) 1432-2013
    ISSN 0031-6768
    DOI 10.1007/s00424-023-02897-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Identification of ATP6V1C2 as a novel candidate gene for distal tubular acidosis.

    Cornière, Nicolas / Eladari, Dominique

    Kidney international

    2020  Volume 97, Issue 3, Page(s) 452–455

    Abstract: Young onset distal tubular acidosis is a rare genetic disorder that can lead, if untreated, to many complications. Mutations in few genes account for almost half of the cases, whereas the molecular mechanisms accounting for the remaining cases are still ... ...

    Abstract Young onset distal tubular acidosis is a rare genetic disorder that can lead, if untreated, to many complications. Mutations in few genes account for almost half of the cases, whereas the molecular mechanisms accounting for the remaining cases are still unknown. The present study reports the use of whole-exome sequencing to identify new dRTA-causing genes and demonstrates that inactivating mutations in the ATP6V1C2 gene impair renal proton pump function.
    MeSH term(s) Acidosis, Renal Tubular ; Humans ; Mutation ; Vacuolar Proton-Translocating ATPases/genetics ; Whole Exome Sequencing
    Chemical Substances Vacuolar Proton-Translocating ATPases (EC 3.6.1.-)
    Language English
    Publishing date 2020-02-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2019.12.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 797: Show issues Location:
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  6. Article ; Online: Renal acid-base regulation: new insights from animal models.

    Eladari, Dominique / Kumai, Yusuke

    Pflugers Archiv : European journal of physiology

    2015  Volume 467, Issue 8, Page(s) 1623–1641

    Abstract: Because majority of biological processes are dependent on pH, maintaining systemic acid-base balance is critical. The kidney contributes to systemic acid-base regulation, by reabsorbing HCO3 (-) (both filtered by glomeruli and generated within a nephron) ...

    Abstract Because majority of biological processes are dependent on pH, maintaining systemic acid-base balance is critical. The kidney contributes to systemic acid-base regulation, by reabsorbing HCO3 (-) (both filtered by glomeruli and generated within a nephron) and acidifying urine. Abnormalities in those processes will eventually lead to a disruption in systemic acid-base balance and provoke metabolic acid-base disorders. Research over the past 30 years advanced our understanding on cellular and molecular mechanisms responsible for those processes. In particular, a variety of transgenic animal models, where target genes are deleted either globally or conditionally, provided significant insights into how specific transporters are contributing to the renal acid-base regulation. Here, we broadly overview the mechanisms of renal ion transport participating to acid-base regulation, with emphasis on data obtained from transgenic mice models.
    MeSH term(s) Animals ; Disease Models, Animal ; Genotype ; Humans ; Kidney/metabolism ; Kidney/physiopathology ; Membrane Transport Proteins/genetics ; Membrane Transport Proteins/metabolism ; Mice, Transgenic ; Models, Biological ; Phenotype ; Renal Elimination ; Renal Reabsorption ; Water-Electrolyte Balance ; Water-Electrolyte Imbalance/genetics ; Water-Electrolyte Imbalance/metabolism ; Water-Electrolyte Imbalance/physiopathology
    Chemical Substances Membrane Transport Proteins
    Language English
    Publishing date 2015-08
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 6380-0
    ISSN 1432-2013 ; 0031-6768
    ISSN (online) 1432-2013
    ISSN 0031-6768
    DOI 10.1007/s00424-014-1669-x
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  7. Article: An emerging role of pendrin in health and disease.

    Kumai, Yusuke / Eladari, Dominique

    Physiological reports

    2015  Volume 3, Issue 8

    Language English
    Publishing date 2015-08
    Publishing country United States
    Document type Editorial
    ZDB-ID 2724325-4
    ISSN 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.12503
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  8. Article ; Online: The Case | Hypokalemia and severe renal loss of sodium.

    Lemoine, Sandrine / Eladari, Dominique / Juillard, Laurent / Bonnefond, Amélie / Froguel, Philippe / Dubourg, Laurence

    Kidney international

    2020  Volume 97, Issue 6, Page(s) 1305–1306

    MeSH term(s) Acidosis, Renal Tubular ; Humans ; Hypokalemia/chemically induced ; Hypokalemia/diagnosis ; Kidney ; Potassium ; Sodium
    Chemical Substances Sodium (9NEZ333N27) ; Potassium (RWP5GA015D)
    Language English
    Publishing date 2020-05-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2019.12.022
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    Zs.A 797: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  9. Article ; Online: Identification of a novel target of thiazide diuretics.

    Eladari, Dominique / Chambrey, Régine

    Journal of nephrology

    2011  Volume 24, Issue 4, Page(s) 391–394

    Abstract: Thiazide diuretics are the older but still one of the most effective therapies for human hypertension. They are believed to act exclusively by blocking renal sodium absorption by the NaCl cotransporter NCC. We recently identified, however, a novel NaCl ... ...

    Abstract Thiazide diuretics are the older but still one of the most effective therapies for human hypertension. They are believed to act exclusively by blocking renal sodium absorption by the NaCl cotransporter NCC. We recently identified, however, a novel NaCl transport system that is expressed in intercalated cells of the collecting duct. This novel mechanism of NaCl transport operates by the combined action of 2 chloride/bicarbonate exchangers, 1 sodium-independent and 1 sodium-dependent. We propose that part of the action of thiazide occurs through blockade of this novel system.
    MeSH term(s) Absorption ; Animals ; Humans ; Hypertension/drug therapy ; Ion Transport/drug effects ; Kidney Tubules, Collecting/drug effects ; Kidney Tubules, Collecting/metabolism ; Mice ; Sodium/pharmacokinetics ; Sodium Chloride/pharmacokinetics ; Sodium Chloride Symporter Inhibitors/pharmacology ; Sodium Chloride Symporters/drug effects
    Chemical Substances Sodium Chloride Symporter Inhibitors ; Sodium Chloride Symporters ; Sodium Chloride (451W47IQ8X) ; Sodium (9NEZ333N27)
    Language English
    Publishing date 2011-07
    Publishing country Italy
    Document type Journal Article
    ZDB-ID 1093991-x
    ISSN 1724-6059 ; 1120-3625 ; 1121-8428
    ISSN (online) 1724-6059
    ISSN 1120-3625 ; 1121-8428
    DOI 10.5301/JN.2011.8403
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3369: Show issues Location:
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  10. Article ; Online: A new mouse model for Bartter's syndrome.

    Teulon, Jacques / Eladari, Dominique

    American journal of physiology. Renal physiology

    2011  Volume 301, Issue 2, Page(s) F295–6

    MeSH term(s) Animals ; Bartter Syndrome/genetics ; Bartter Syndrome/metabolism ; Chloride Channels/metabolism ; Disease Models, Animal ; Membrane Proteins/genetics ; Mice ; Mice, Transgenic ; Phenotype
    Chemical Substances Bsnd protein, mouse ; Chloride Channels ; Clcnka protein, mouse ; Membrane Proteins
    Language English
    Publishing date 2011-08
    Publishing country United States
    Document type Comment ; Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00286.2011
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