Evidence map›Paper›PMID 30895336›Full record

ArticleCellular and molecular life sciences : CMLS2019

A role for polycystin-1 and polycystin-2 in neural progenitor cell differentiation.

Natalie Winokurow, Stefan Schumacher

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 11 citations in OpenAlex.

  1. Polycystin-1 Controls Cell Cycle Kinetics, Cell Cycle Exit, and Differentiation of Neural Progenitor Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Article
  3. Review
  4. Calcium and Neural Stem Cell Proliferation.International journal of molecular sciences · 2024
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. The role of motile cilia in the development and physiology of the nervous system.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Review
  10. Article
  11. Article
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

2 authors at 1 institution in 1 country.

Natalie WinokurowInstitute of Molecular and Cellular Anatomy, Ulm University, Albert-Einstein-Allee 11, 89081, Ulm, Germany.
Stefan SchumacherInstitute of Molecular and Cellular Anatomy, Ulm University, Albert-Einstein-Allee 11, 89081, Ulm, Germany. stefan.schumacher@uni-ulm.de.
Universität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Polycystin-1 (PC1) and polycystin-2 (PC2) are transmembrane proteins encoded by the Pkd1 and Pkd2 genes, respectively. Mutations in these genes are causative for the development of autosomal-dominant polycystic kidney disease. A prominent feature of this disease is an unbalanced cell proliferation. PC1 and PC2 physically interact to form a complex, which localizes to the primary cilia of renal epithelial cells. Recently, PC1 and PC2 have also been described to be present in primary cilia of radial glial cells (RGCs) and to contribute to the planar cell polarity of late RGCs and E1 ependymal cells. As neural progenitor cells (NPCs), early RGCs have to balance proliferation for expansion, or for self-renewal and differentiation to generate neurons. It is not known whether the polycystins play a role in this process. Here, we show that PC1 and PC2 are expressed in RGCs of the developing mouse cerebral cortex during neurogenesis. Loss-of-function analysis and cell-based assays reveal that a reduction of PC1 or PC2 expression leads to increased NPC proliferation, while the differentiation to neurons becomes impaired. The increased NPC proliferation is preceded by enhanced Notch signaling and accompanied by a rise in the number of symmetric cell divisions. The transcription factor STAT3 seems to be mechanistically important for polycystin signaling in NPCs as either STAT3 knockdown or inhibition of STAT3 function abrogates the increased proliferation driven by reduced polycystin expression. Our findings indicate that PC1 and PC2 are critical for maintaining a balance between proliferation and differentiation of NPCs.

Indexed as

Cell DifferentiationNeurogenesisCell ProliferationCells, CulturedEpendymoglial CellsHumansNeural Stem CellsSignal TransductionTRPP Cation ChannelsTRPP Cation ChannelsBrdU labelingCBFRE sensorMAP2NestinVentricular zone

Identifiers

PMID30895336
PMCPMC11105687
OpenAlexW2923134471

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.