Evidence map›Paper›PMID 21949092›Full record

ArticleJournal of the American Society of Nephrology : JASN2011

Glcci1 deficiency leads to proteinuria.

Yukino Nishibori, Kan Katayama, Mataleena Parikka, Asmundur Oddsson, Masatoshi Nukui, Kjell Hultenby, Annika Wernerson, Bing He, Lwaki Ebarasi, Elisabeth Raschperger and 5 more

Open access · greenAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Reduced α-galactosidase A activity in zebrafish (Molecular genetics and metabolism reports · 2022
    Article
  5. Review
  6. Indirect podocyte injury manifested in a partial podocytectomy mouse model.American journal of physiology. Renal physiology · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Characterization of Glcci1 expression in a subpopulation of lateral ganglionic eminence progenitors in the mouse telencephalon.Developmental dynamics : an official publication of the American Association of Anatomists · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Defining nephrotic syndrome from an integrative genomics perspective.Pediatric nephrology (Berlin, Germany) · 2015
    Review
  16. Article
  17. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 1 country.

Yukino NishiboriDepartment of Medical Biochemistry and Biophysics, Division of Matrix Biology, Karolinska Institutet, 171 77 Stockholm, Sweden.
Kan Katayama
Mataleena Parikka
Asmundur Oddsson
Masatoshi Nukui
Kjell Hultenby
Annika Wernerson
Bing He
Lwaki Ebarasi
Elisabeth Raschperger
Jenny Norlin
Mathias Uhlén
Jaakko Patrakka
Christer Betsholtz
Karl Tryggvason
Karolinska Institutet · SEKTH Royal Institute of Technology · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unbiased transcriptome profiling and functional genomics approaches identified glucocorticoid-induced transcript 1 (GLCCI1) as being a transcript highly specific for the glomerulus, but its role in glomerular development and disease is unknown. Here, we report that mouse glomeruli express far greater amounts of Glcci1 protein compared with the rest of the kidney. RT-PCR and Western blotting demonstrated that mouse glomerular Glcci1 is approximately 60 kD and localizes to the cytoplasm of podocytes in mature glomeruli. In the fetal kidney, intense Glcci1 expression occurs at the capillary-loop stage of glomerular development. Using gene knockdown in zebrafish with morpholinos, morphants lacking Glcci1 function had collapsed glomeruli with foot-process effacement. Permeability studies of the glomerular filtration barrier in these zebrafish morphants demonstrated a disruption of the selective glomerular permeability filter. Taken together, these data suggest that Glcci1 promotes the normal development and maintenance of podocyte structure and function.

Indexed as

AnimalsCytoplasmDexamethasoneDisease Models, AnimalGene Expression Regulation, DevelopmentalGlucocorticoidsKidney GlomerulusMaleMiceMice, Inbred ICROligonucleotides, AntisensePodocytesPronephrosProteinuriaRabbitsReceptors, GlucocorticoidDexamethasoneglcci1a protein, zebrafishglucocorticoid-induced transcript 1 protein, mouseGlucocorticoidsOligonucleotides, AntisenseReceptors, GlucocorticoidZebrafish Proteins

Identifiers

PMID21949092
PMCPMC3279996
OpenAlexW2128177072

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.