Evidence map›Paper›PMID 20861303›Full record

ArticleMolecular biology of the cell2010

MAL/VIP17, a new player in the regulation of NKCC2 in the kidney.

Monica Carmosino, Federica Rizzo, Giuseppe Procino, Davide Basco, Giovanna Valenti, Biff Forbush, Nicole Schaeren-Wiemers, Michael J Caplan, Maria Svelto

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. TRPML1-Induced Lysosomal CaInternational journal of molecular sciences · 2023
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Molecular regulation of NKCC2 in blood pressure control and hypertension.Current opinion in nephrology and hypertension · 2019
    Review
  10. Article
  11. Regulation of renal Na-(K)-Cl cotransporters by vasopressin.Pflugers Archiv : European journal of physiology · 2017
    Review
  12. Article
  13. Article
  14. Physiology and pathophysiology of SLC12A1/2 transporters.Pflugers Archiv : European journal of physiology · 2014
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. VIP17/MAL expression modulates epithelial cyst formation and ciliogenesis.American journal of physiology. Cell physiology · 2012
    Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Monica CarmosinoDepartment of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06511, USA. carmosino@yale.edu
Federica Rizzo
Giuseppe Procino
Davide Basco
Giovanna Valenti
Biff Forbush
Nicole Schaeren-Wiemers
Michael J Caplan
Maria Svelto
University of Bari Aldo Moro · ITYale University · USUniversity Hospital of Basel · CH

Funding

Pathways and Partners in Renal Epithelial Cell PolarityR01DK072614 · NIDDK · YALE UNIVERSITY · PI CAPLAN, MICHAEL J. · 2005 to 2022
$6.9M
NIDDK NIH HHS R01 DK072614
6 · The paper itself

Abstract

The renal-specific Na+-K+-2Cl- cotransporter (NKCC2) is the major salt transport pathway of the apical membrane of the mammalian thick ascending limb of Henle's loop. Here, we analyze the role of the tetraspan protein myelin and lymphocytes-associated protein (MAL)/VIP17 in the regulation of NKCC2. We demonstrated that 1) NKCC2 and MAL/VIP17 colocalize and coimmunoprecipitate in Lilly Laboratories cell porcine kidney cells (LLC-PK1) as well as in rat kidney medullae, 2) a 150-amino acid stretch of NKCC2 C-terminal tail is involved in the interaction with MAL/VIP17, 3) MAL/VIP17 increases the cell surface retention of NKCC2 by attenuating its internalization, and 4) this coincides with an increase in cotransporter phosphorylation. Interestingly, overexpression of MAL/VIP17 in the kidney of transgenic mice results in cysts formation in distal nephron structures consistent with the hypothesis that MAL/VIP17 plays an important role in apical sorting or in maintaining the stability of the apical membrane. The NKCC2 expressed in these mice was highly glycosylated and phosphorylated, suggesting that MAL/VIP17 also is involved in the stabilization of NKCC2 at the apical membrane in vivo. Thus, the involvement of MAL/VIP17 in the activation and surface expression of NKCC2 could play an important role in the regulated absorption of Na+ and Cl- in the kidney.

Indexed as

AnimalsBlotting, WesternCell LineEndocytosisEpithelial CellsHumansImmunoprecipitationKidneyLLC-PK1 CellsMembrane Transport ProteinsMiceMice, TransgenicMyelin and Lymphocyte-Associated Proteolipid ProteinsMyelin ProteinsPhosphorylationProtein BindingMAL protein, humanMal protein, mouseMal protein, ratMembrane Transport ProteinsMyelin and Lymphocyte-Associated Proteolipid ProteinsMyelin ProteinsProteolipidsSLC12A1 protein, humanSlc12a1 protein, mouseSlc12a1 protein, ratSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1

Identifiers

PMID20861303
PMCPMC2982131
OpenAlexW2171151713

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LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

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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.