Evidence map›Paper›PMID 30514723›Full record

ArticleJournal of the American Society of Nephrology : JASN2019

Endogenous Notch Signaling in Adult Kidneys Maintains Segment-Specific Epithelial Cell Types of the Distal Tubules and Collecting Ducts to Ensure Water Homeostasis.

Malini Mukherjee, Jennifer deRiso, Karla Otterpohl, Ishara Ratnayake, Divya Kota, Phil Ahrenkiel, Indra Chandrasekar, Kameswaran Surendran

Abstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

  1. Hmx2 and Dmrt2 Coordinate the Differentiation of Intercalated Cell Subtypes in Kidney.Journal of the American Society of Nephrology : JASN · 2026
    Article
  2. Cell-cell crosstalk in kidney health and disease.Nature reviews. Nephrology · 2026
    Review
  3. Review
  4. Pendrin is upregulated by corticosterone and participates in its pressor response.American journal of physiology. Renal physiology · 2026
    Article
  5. Article
  6. Lineage tracing reveals KSPFrontiers in cell and developmental biology · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Absence of E-Cadherin and β-Catenin in the Basal Plasma Membrane of Collecting Duct Cells During NDI Development and Recovery.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Malini MukherjeePediatrics and Rare Diseases Group and.
Jennifer deRisoPediatrics and Rare Diseases Group and.
Karla OtterpohlEnabling Technologies Group, Sanford Research, Sioux Falls, South Dakota.
Ishara RatnayakeDepartment of Nanoscience and Nanoengineering, South Dakota School of Mines and Technology, Rapid City, South Dakota; and.
Divya KotaDepartment of Nanoscience and Nanoengineering, South Dakota School of Mines and Technology, Rapid City, South Dakota; and.
Phil AhrenkielDepartment of Nanoscience and Nanoengineering, South Dakota School of Mines and Technology, Rapid City, South Dakota; and.
Indra ChandrasekarEnabling Technologies Group, Sanford Research, Sioux Falls, South Dakota.
Kameswaran SurendranPediatrics and Rare Diseases Group and kameswaran.surendran@sanfordhealth.org.
South Dakota School of Mines and Technology · USUniversity of South Dakota · USSanford Research · US

Funding

Yeast 2 HybridP20GM103620 · NIGMS · SANFORD RESEARCH/USD · PI ROUX, KYLE J · 2013 to 2023
$24.2M
Transdisciplinary approaches to American Indian and rural population health researchP20GM121341 · NIGMS · SANFORD RESEARCH/USD · PI ANGAL, JYOTI · 2017 to 2022
$11.8M
Molecular Regulators of Renal Collecting Duct Differentiation and MaintenanceR01DK106135 · NIDDK · SANFORD RESEARCH/USD · PI SURENDRAN, KAMESWARAN · 2016 to 2019
$1.5M
NIDDK NIH HHS R01 DK106135NIGMS NIH HHS P20 GM103620NIGMS NIH HHS P20 GM121341
6 · The paper itself

Abstract

backgroundNotch signaling is required during kidney development for nephron formation and principal cell fate selection within the collecting ducts. Whether Notch signaling is required in the adult kidney to maintain epithelial diversity, or whether its loss can trigger principal cell transdifferentiation (which could explain acquired diabetes insipidus in patients receiving lithium) is unclear.

methodsTo investigate whether loss of Notch signaling can trigger principal cells to lose their identity, we genetically inactivated

resultsNotch signaling was required for maintenance of Aqp2-expressing cells in distal nephron and collecting duct segments in adult kidneys. Fate tracing revealed mature principal cells in the inner stripe of the outer medulla converted to intercalated cells after genetic inactivation of

conclusionsNotch signaling

Indexed as

AnimalsAquaporin 2Cell DifferentiationCells, CulturedEpithelial CellsHomeostasisKidneyKidney Tubules, CollectingLithiumMiceReceptor, Notch1Receptor, Notch2Signal TransductionWater-Electrolyte BalanceAquaporin 2LithiumReceptor, Notch1Receptor, Notch2collecting ductintercalatedionocyteNotch Signalingprincipaltransdifferentiation

Identifiers

PMID30514723
PMCPMC6317606
OpenAlexW2902476811

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.