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  1. Article ; Online: The role of Cl

    Koumangoye, Rainelli

    American journal of physiology. Cell physiology

    2022  Volume 322, Issue 4, Page(s) C645–C652

    Abstract: Inflammation is part of innate immunity and is a natural response of the body to bacteria, virus, and any other pathogen infections or to damaged tissues. However, too much inflammation or chronic inflammation contributes to a wide variety of diseases ... ...

    Abstract Inflammation is part of innate immunity and is a natural response of the body to bacteria, virus, and any other pathogen infections or to damaged tissues. However, too much inflammation or chronic inflammation contributes to a wide variety of diseases such as inflammatory bowel disease, cancer, type 2 diabetes, heart disease, and autoimmune diseases such as rheumatoid arthritis. Recent studies underscored the critical role of K
    MeSH term(s) Chlorides/metabolism ; Diabetes Mellitus, Type 2 ; Humans ; Immunity, Innate ; Inflammasomes/metabolism ; Inflammation/genetics ; Interleukin-1beta/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Potassium/metabolism
    Chemical Substances Chlorides ; Inflammasomes ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein ; Potassium (RWP5GA015D)
    Language English
    Publishing date 2022-02-16
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00421.2021
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  2. Article ; Online: NKCC1 in human diseases: is the

    Delpire, Eric / Koumangoye, Rainelli

    American journal of physiology. Cell physiology

    2023  Volume 325, Issue 2, Page(s) C385–C390

    Abstract: Mutations in ... ...

    Abstract Mutations in the
    MeSH term(s) Humans ; Mice ; Animals ; Female ; Symporters/genetics ; Sodium-Potassium-Chloride Symporters/genetics ; Solute Carrier Family 12, Member 2/genetics ; Mice, Knockout ; Mutation/genetics ; Deafness
    Chemical Substances Symporters ; Sodium-Potassium-Chloride Symporters ; Solute Carrier Family 12, Member 2 ; SLC12A2 protein, human
    Language English
    Publishing date 2023-07-03
    Publishing country United States
    Document type Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Journal Article
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00238.2023
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  3. Article ; Online: Kinase Scaffold Cab39 Is Necessary for Phospho-Activation of the Thiazide-Sensitive NCC.

    Ferdaus, Mohammed Z / Koumangoye, Rainelli B / Welling, Paul A / Delpire, Eric

    Hypertension (Dallas, Tex. : 1979)

    2024  Volume 81, Issue 4, Page(s) 801–810

    Abstract: Background: Potassium regulates the WNK (with no lysine kinase)-SPAK (STE20/SPS1-related proline/alanine-rich kinase) signaling axis, which in turn controls the phosphorylation and activation of the distal convoluted tubule thiazide-sensitive NCC ( ... ...

    Abstract Background: Potassium regulates the WNK (with no lysine kinase)-SPAK (STE20/SPS1-related proline/alanine-rich kinase) signaling axis, which in turn controls the phosphorylation and activation of the distal convoluted tubule thiazide-sensitive NCC (sodium-chloride cotransporter) for sodium-potassium balance. Although their roles in the kidney have not been investigated, it has been postulated that Cab39 (calcium-binding protein 39) or Cab39l (Cab39-like) is required for SPAK/OSR1 (oxidative stress response 1) activation. This study demonstrates how they control the WNK-SPAK/OSR1-NCC pathway.
    Methods: We created a global knockout of Cab39l and a tamoxifen-inducible, NCC-driven, Cab39 knockout. The 2 lines were crossed to generate Cab39-DKO (Cab39 double knockout) animals. Mice were studied under control and low-potassium diet, which activates WNK-SPAK/OSR1-NCC phosphorylation. Western blots were used to assess the expression and phosphorylation of proteins. Blood and urine electrolytes were measured to test for compromised NCC function. Immunofluorescence studies were conducted to localize SPAK and OSR1.
    Results: Both Cab39l and Cab39 are expressed in distal convoluted tubule, and only the elimination of both leads to a striking absence of NCC phosphorylation. Cab39-DKO mice exhibited a loss-of-NCC function, like in Gitelman syndrome. In contrast to the apical membrane colocalization of SPAK with NCC in wild-type mice, SPAK and OSR1 become confined to intracellular puncta in the Cab39-DKO mice.
    Conclusions: In the absence of Cab39 proteins, NCC cannot be phosphorylated, resulting in a Gitelman-like phenotype. Cab39 proteins function to localize SPAK at the apical membrane with NCC, reminiscent of the Cab39 yeast homolog function, translocating kinases during cytokinesis.
    MeSH term(s) Mice ; Animals ; Protein Serine-Threonine Kinases/genetics ; Protein Serine-Threonine Kinases/metabolism ; Solute Carrier Family 12, Member 3/genetics ; Solute Carrier Family 12, Member 3/metabolism ; Thiazides/pharmacology ; Phosphorylation ; Kidney Tubules, Distal/metabolism ; Potassium/metabolism
    Chemical Substances Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Solute Carrier Family 12, Member 3 ; Thiazides ; Potassium (RWP5GA015D)
    Language English
    Publishing date 2024-01-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.123.22464
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  4. Article ; Online: Loss of NKCC1 function increases epithelial tight junction permeability by upregulating claudin-2 expression.

    Koumangoye, Rainelli / Penny, Parker / Delpire, Eric

    American journal of physiology. Cell physiology

    2022  Volume 323, Issue 4, Page(s) C1251–C1263

    Abstract: Conditions that cause the loss of epithelial barrier integrity are often accompanied by dysregulation of tight junction protein expression and/or localization. Recently, we have reported that patients with mutations ... ...

    Abstract Conditions that cause the loss of epithelial barrier integrity are often accompanied by dysregulation of tight junction protein expression and/or localization. Recently, we have reported that patients with mutations in
    MeSH term(s) Cations/metabolism ; Claudin-2/genetics ; Claudin-2/metabolism ; Dextrans/metabolism ; Fluoresceins/metabolism ; Humans ; Inflammation/metabolism ; Intestinal Mucosa/metabolism ; Occludin/genetics ; Occludin/metabolism ; Permeability ; Solute Carrier Family 12, Member 2/genetics ; Solute Carrier Family 12, Member 2/metabolism ; Tight Junction Proteins/metabolism ; Tight Junctions/metabolism
    Chemical Substances Cations ; Claudin-2 ; Dextrans ; Fluoresceins ; Occludin ; SLC12A2 protein, human ; Solute Carrier Family 12, Member 2 ; Tight Junction Proteins
    Language English
    Publishing date 2022-08-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00334.2022
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  5. Article ; Online: Bicarbonate is the primary inducer of KCC3a expression in renal cortical B-type intercalated cells.

    Ferdaus, Mohammed Z / Terker, Andrew S / Koumangoye, Rainelli / Wall, Susan M / Delpire, Eric

    American journal of physiology. Cell physiology

    2023  Volume 324, Issue 5, Page(s) C1171–C1178

    Abstract: A primary function of intercalated cells in the distal tubule of the kidney is to maintain pH homeostasis. For example, type B intercalated cells secrete bicarbonate largely through the action of the apical ... ...

    Abstract A primary function of intercalated cells in the distal tubule of the kidney is to maintain pH homeostasis. For example, type B intercalated cells secrete bicarbonate largely through the action of the apical Cl
    MeSH term(s) Animals ; Mice ; Bicarbonates/metabolism ; Aldosterone/pharmacology ; Aldosterone/metabolism ; Angiotensin II/pharmacology ; Angiotensin II/metabolism ; Kidney/metabolism ; Sulfate Transporters/genetics ; Sulfate Transporters/metabolism ; Alkalosis/metabolism ; Anion Transport Proteins/genetics
    Chemical Substances Bicarbonates ; Aldosterone (4964P6T9RB) ; Angiotensin II (11128-99-7) ; Sulfate Transporters ; Anion Transport Proteins
    Language English
    Publishing date 2023-04-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00094.2023
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  6. Article: KCC3a, a Strong Candidate Pathway for K

    Ferdaus, Mohammed Zubaerul / Terker, Andrew Scott / Koumangoye, Rainelli / Delpire, Eric

    Frontiers in cell and developmental biology

    2022  Volume 10, Page(s) 931326

    Abstract: Loss-of-function mutations in the human potassium chloride cotransporter-3 (KCC3) cause a hereditary motor sensory neuropathy associated with agenesis of the corpus callosum. While recapitulating the neuropathy, KCC3-knockout mice also exhibit high blood ...

    Abstract Loss-of-function mutations in the human potassium chloride cotransporter-3 (KCC3) cause a hereditary motor sensory neuropathy associated with agenesis of the corpus callosum. While recapitulating the neuropathy, KCC3-knockout mice also exhibit high blood pressure. This phenotype is believed to have neurogenic and/or vascular origins. The role of KCC3 in the kidney is poorly understood. KCC3 is encoded by two major isoforms originating from alternative promoters: KCC3a and KCC3b, with KCC3b being the predominant transcript in the kidney. Although the transporter has previously been localized to the proximal tubule, we show here the unique expression of the KCC3a isoform in the connecting tubule. Using a KCC3a-specific polyclonal antibody validated for both immunofluorescence and immunoblotting, we showed an intense KCC3a signal restricted to cortical intercalated cells. No overlap is detected between KCC3a and sodium chloride cotransporter (NCC), a distal convoluted tubule (DCT) marker; or between KCC3a and ENaC or calbindin, which are both principal cell markers. KCC3a signal was observed in cells expressing the apical V-ATPase and pendrin, establishing a unique expression pattern characteristic of intercalated cells of type-B or type-nonA/nonB. We further show that treatment of wild-type mice with hydrochlorothiazide, amiloride, or fed a K
    Language English
    Publishing date 2022-07-07
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.931326
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  7. Article ; Online: NKCC1: Newly Found as a Human Disease-Causing Ion Transporter.

    Koumangoye, Rainelli / Bastarache, Lisa / Delpire, Eric

    Function (Oxford, England)

    2020  Volume 2, Issue 1, Page(s) zqaa028

    Abstract: Among the electroneutral ... ...

    Abstract Among the electroneutral Na
    MeSH term(s) Animals ; Child ; Humans ; Mice ; Alleles ; Membrane Transport Proteins/genetics ; Mice, Knockout ; Mutation ; Sodium/metabolism ; Solute Carrier Family 12, Member 2/genetics
    Chemical Substances Membrane Transport Proteins ; SLC12A2 protein, human ; Sodium (9NEZ333N27) ; Solute Carrier Family 12, Member 2
    Language English
    Publishing date 2020-11-03
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2633-8823
    ISSN (online) 2633-8823
    DOI 10.1093/function/zqaa028
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  8. Article ; Online: KCC3a, a Strong Candidate Pathway for K+ Loss in Alkalemia

    Mohammed Zubaerul Ferdaus / Andrew Scott Terker / Rainelli Koumangoye / Eric Delpire

    Frontiers in Cell and Developmental Biology, Vol

    2022  Volume 10

    Abstract: Loss-of-function mutations in the human potassium chloride cotransporter-3 (KCC3) cause a hereditary motor sensory neuropathy associated with agenesis of the corpus callosum. While recapitulating the neuropathy, KCC3-knockout mice also exhibit high blood ...

    Abstract Loss-of-function mutations in the human potassium chloride cotransporter-3 (KCC3) cause a hereditary motor sensory neuropathy associated with agenesis of the corpus callosum. While recapitulating the neuropathy, KCC3-knockout mice also exhibit high blood pressure. This phenotype is believed to have neurogenic and/or vascular origins. The role of KCC3 in the kidney is poorly understood. KCC3 is encoded by two major isoforms originating from alternative promoters: KCC3a and KCC3b, with KCC3b being the predominant transcript in the kidney. Although the transporter has previously been localized to the proximal tubule, we show here the unique expression of the KCC3a isoform in the connecting tubule. Using a KCC3a-specific polyclonal antibody validated for both immunofluorescence and immunoblotting, we showed an intense KCC3a signal restricted to cortical intercalated cells. No overlap is detected between KCC3a and sodium chloride cotransporter (NCC), a distal convoluted tubule (DCT) marker; or between KCC3a and ENaC or calbindin, which are both principal cell markers. KCC3a signal was observed in cells expressing the apical V-ATPase and pendrin, establishing a unique expression pattern characteristic of intercalated cells of type-B or type-nonA/nonB. We further show that treatment of wild-type mice with hydrochlorothiazide, amiloride, or fed a K+-deficient diet up-regulates KCC3a level, suggesting that volume depletion increases KCC3a abundance. This hypothesis was confirmed by showing a higher abundance of KCC3a protein after 23-h water restriction or after placing the mice on a low-salt diet. More importantly, abundance of the Cl−/HCO3− exchanger, pendrin, which is known to secrete bicarbonate in alkalotic conditions, was significantly diminished in KCC3-knockout mice. In addition, KCC3a abundance increased significantly alongside pendrin abundance in bicarbonate-treated alkalotic mice, providing a credible mechanism for K+ loss in metabolic alkalosis.
    Keywords K–Cl cotransport ; intercalated cells ; bicarbonate ; metabolic alkalosis ; K+ loss ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2022-07-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: A mutation in the Na-K-2Cl cotransporter-1 leads to changes in cellular metabolism.

    Omer, Salma / Koumangoye, Rainelli / Delpire, Eric

    Journal of cellular physiology

    2020  Volume 235, Issue 10, Page(s) 7239–7250

    Abstract: The Na-K-Cl cotransporter-1 (NKCC1), by mediating the electroneutral transport of ... ...

    Abstract The Na-K-Cl cotransporter-1 (NKCC1), by mediating the electroneutral transport of Na
    MeSH term(s) Adolescent ; Animals ; Cell Line ; DNA, Mitochondrial/metabolism ; Dogs ; Energy Metabolism/genetics ; Female ; Fibroblasts/metabolism ; Glycolysis ; Humans ; Madin Darby Canine Kidney Cells ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Microscopy, Electron, Transmission ; Mitochondria/metabolism ; Mitochondria/ultrastructure ; Multiple Organ Failure/genetics ; Multiple Organ Failure/metabolism ; Mutant Proteins/chemistry ; Mutant Proteins/genetics ; Mutant Proteins/metabolism ; Mutation ; Recombinant Fusion Proteins/chemistry ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/metabolism ; Sequence Deletion ; Solute Carrier Family 12, Member 2/chemistry ; Solute Carrier Family 12, Member 2/genetics ; Solute Carrier Family 12, Member 2/metabolism
    Chemical Substances DNA, Mitochondrial ; Mutant Proteins ; Recombinant Fusion Proteins ; SLC12A2 protein, human ; Slc12a2 protein, mouse ; Solute Carrier Family 12, Member 2
    Language English
    Publishing date 2020-02-10
    Publishing country United States
    Document type Case Reports ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.29623
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  10. Article ; Online: DNPEP is not the only peptidase that produces SPAK fragments in kidney.

    Koumangoye, Rainelli / Delpire, Eric

    Physiological reports

    2017  Volume 5, Issue 21

    Abstract: SPAK (STE20/SPS1-related proline/alanine-rich kinase) regulates ... ...

    Abstract SPAK (STE20/SPS1-related proline/alanine-rich kinase) regulates Na
    MeSH term(s) Animals ; CRISPR-Cas Systems ; Female ; Glutamyl Aminopeptidase/metabolism ; Kidney/enzymology ; Male ; Mice ; Mice, Knockout ; Peptide Hydrolases/metabolism ; Protein-Serine-Threonine Kinases/metabolism
    Chemical Substances Stk39 protein, mouse (EC 2.7.1.-) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Peptide Hydrolases (EC 3.4.-) ; Glutamyl Aminopeptidase (EC 3.4.11.7)
    Language English
    Publishing date 2017-11-09
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.13479
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