Evidence map›Paper›PMID 26574044›Full record

ArticleJournal of the American Society of Nephrology : JASN2016

Defective Store-Operated Calcium Entry Causes Partial Nephrogenic Diabetes Insipidus.

Mykola Mamenko, Isha Dhande, Viktor Tomilin, Oleg Zaika, Nabila Boukelmoune, Yaming Zhu, Manuel L Gonzalez-Garay, Oleh Pochynyuk, Peter A Doris

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Calcium signalling and transport in the kidney.Nature reviews. Nephrology · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. TRPML1-Induced Lysosomal CaInternational journal of molecular sciences · 2023
    Article
  7. Expression Regulation and Trafficking of Aquaporins.Advances in experimental medicine and biology · 2023
    Review
  8. Intracellular CaFrontiers in physiology · 2023
    Review
  9. Insight into the Mammalian Aquaporin Interactome.International journal of molecular sciences · 2022
    Review
  10. ClC-K2 ClFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  11. Hypercalciuria switches CaGenes & diseases · 2022
    Article
  12. Store-operated calcium entry: Pivotal roles in renal physiology and pathophysiology.Experimental biology and medicine (Maywood, N.J.) · 2021
    Review
  13. Review
  14. Review
  15. Article
  16. Journal of the American Heart Association · 2020
    Article
  17. Article
  18. Urinary concentrating defect in mice lacking Epac1 or Epac2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 3 countries.

Mykola MamenkoDepartment of Integrative Biology and Pharmacology, and.
Isha DhandeInstitute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, Texas; and.
Viktor TomilinDepartment of Integrative Biology and Pharmacology, and Institute of Cytology, Russian Academy of Sciences, St. Petersburg, Russia.
Oleg ZaikaDepartment of Integrative Biology and Pharmacology, and.
Nabila BoukelmouneDepartment of Integrative Biology and Pharmacology, and.
Yaming ZhuInstitute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, Texas; and.
Manuel L Gonzalez-GarayInstitute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, Texas; and.
Oleh PochynyukDepartment of Integrative Biology and Pharmacology, and peter.a.doris@uth.tmc.edu Oleh.M.Pochynyuk@uth.tmc.edu.
Peter A DorisInstitute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, Texas; and peter.a.doris@uth.tmc.edu Oleh.M.Pochynyuk@uth.tmc.edu.
Laboratoire d’immunologie intégrative du cancer · FRThe University of Texas Health Science Center at Houston · USInstitute of Cytology · RU

Funding

Hypertensive Renal InjuryR01DK081866 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DORIS, PETER A · 2009 to 2017
$2.9M
Aldosterone-independent regulation of ENaC by systemic saltR01DK095029 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI POCHYNYUK, OLEH · 2012 to 2016
$1.6M
HNF1 transcriptional control of renal oxidative stressR01DK069632 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DORIS, PETER A · 2005 to 2009
$1.4M
Hypertensive Renal InjuryR56DK081866 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DORIS, PETER A · 2012 to 2012
$100k
NIDDK NIH HHS R01 DK069632NIDDK NIH HHS R01 DK081866NIDDK NIH HHS R01 DK095029NIDDK NIH HHS R56 DK081866
6 · The paper itself

Abstract

Store-operated calcium entry (SOCE) is the mechanism by which extracellular signals elicit prolonged intracellular calcium elevation to drive changes in fundamental cellular processes. Here, we investigated the role of SOCE in the regulation of renal water reabsorption, using the inbred rat strain SHR-A3 as an animal model with disrupted SOCE. We found that SHR-A3, but not SHR-B2, have a novel truncating mutation in the gene encoding stromal interaction molecule 1 (STIM1), the endoplasmic reticulum calcium (Ca(2+)) sensor that triggers SOCE. Balance studies revealed increased urine volume, hypertonic plasma, polydipsia, and impaired urinary concentrating ability accompanied by elevated circulating arginine vasopressin (AVP) levels in SHR-A3 compared with SHR-B2. Isolated, split-open collecting ducts (CD) from SHR-A3 displayed decreased basal intracellular Ca(2+) levels and a major defect in SOCE. Consequently, AVP failed to induce the sustained intracellular Ca(2+) mobilization that requires SOCE in CD cells from SHR-A3. This effect decreased the abundance of aquaporin 2 and enhanced its intracellular retention, suggesting impaired sensitivity of the CD to AVP in SHR-A3. Stim1 knockdown in cultured mpkCCDc14 cells reduced SOCE and basal intracellular Ca(2+) levels and prevented AVP-induced translocation of aquaporin 2, further suggesting the effects in SHR-A3 result from the expression of truncated STIM1. Overall, these results identify a novel mechanism of nephrogenic diabetes insipidus and uncover a role of SOCE in renal water handling.

Indexed as

AnimalsAquaporin 2Arginine VasopressinCalcium ChannelsCells, CulturedDiabetes Insipidus, NephrogenicMaleRatsRats, Inbred SHRStromal Interaction Molecule 1Aquaporin 2Arginine VasopressinCalcium ChannelsStim1 protein, ratStromal Interaction Molecule 1calciumcollecting ductsdiabetes insipidusvasopressinwater transport

Identifiers

PMID26574044
PMCPMC4926963
OpenAlexW2212814597

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.