Evidence map›Paper›PMID 11106563›Full record

ArticleThe American journal of pathology2000

Role of nephrin in cell junction formation in human nephrogenesis.

V Ruotsalainen, J Patrakka, P Tissari, P Reponen, M Hess, M Kestilä, C Holmberg, R Salonen, M Heikinheimo, J Wartiovaara and 2 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

43 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
  2. Article
  3. Podocytes in health and glomerular disease.Frontiers in cell and developmental biology · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Complexities of the glomerular basement membrane.Nature reviews. Nephrology · 2021
    Review
  9. Article
  10. Article
  11. GPRC5b Modulates Inflammatory Response in Glomerular DiseasesJournal of the American Society of Nephrology : JASN · 2019
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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

12 authors at 5 institutions in 3 countries.

V RuotsalainenBiocenter and Department of Biochemistry, University of Oulu, Oulu, Finland. University of Helsinki, Finland.
J Patrakka
P Tissari
P Reponen
M Hess
M Kestilä
C Holmberg
R Salonen
M Heikinheimo
J Wartiovaara
K Tryggvason
H Jalanko
University of Helsinki · FIBiocenter Finland · FIKarolinska Institutet · SEOulu University Hospital · FIUniversity of Oulu · FI

Funding

NEPHRIN AND KIDNEY FUNCTION AND DISEASER01DK054724 · NIDDK · KAROLINSKA INSTITUTE · PI TRYGGVASON, KARL · 1999 to 2001
$368k
NIDDK NIH HHS DK54724
6 · The paper itself

Abstract

Nephrin is a cell adhesion protein located at the slit diaphragm area of glomerular podocytes. Mutations in nephrin-coding gene (NPHS1) cause congenital nephrotic syndrome (NPHS1). We studied the developmental expression of nephrin, ZO-1 and P-cadherin in normal fetal kidneys and in NPHS1 kidneys. We used in situ hybridization and immunohistochemistry at light and electron microscopic levels. Nephrin and zonula occludens-1 (ZO-1) were first expressed in late S-shaped bodies. During capillary loop stage, nephrin and ZO-1 localized at the basal margin and in the cell-cell adhesion sites between developing podocytes, especially in junctions with ladder-like structures. In mature glomeruli, nephrin and ZO-1 concentrated at the slit diaphragm area. P-cadherin was first detected in ureteric buds, tubules, and vesicle stage glomeruli. Later, P-cadherin was seen at the basal margin of developing podocytes. Fetal NPHS1 kidneys with Fin-major/Fin-major genotype did not express nephrin, whereas the expression of ZO-1 and P-cadherin was comparable to that of control kidneys. Although early junctional complexes proved structurally normal, junctions with ladder-like structures and slit diaphragms were completely missing. The results indicate that nephrin is dispensable for early development of podocyte junctional complexes. However, nephrin appears to be essential for formation of junctions with ladder-like structures and slit diaphragms.

Indexed as

CadherinsEmbryonic and Fetal DevelopmentFetusHumansIntercellular JunctionsKidneyKidney GlomerulusMembrane ProteinsMicroscopy, ImmunoelectronMutationPhosphoproteinsProteinsReference ValuesZonula Occludens-1 ProteinCadherinsMembrane ProteinsnephrinPhosphoproteinsProteinsTJP1 protein, humanZonula Occludens-1 Protein

Identifiers

PMID11106563
PMCPMC1885750
OpenAlexW2077980938

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.