Evidence map›Paper›PMID 19013236›Full record

ReviewBiochimica et biophysica acta2009

Familial tumoral calcinosis and the role of O-glycosylation in the maintenance of phosphate homeostasis.

Ilana Chefetz, Eli Sprecher

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2009. 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
2.6field-weighted citation impact, top 10% 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, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Proteomic analysis of diabetic retinas.Frontiers in endocrinology · 2023
    Article
  4. Effects of ferric citrate and intravenous iron sucrose on markers of mineral, bone, and iron homeostasis in a rat model of CKD-MBD.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2022
    Article
  5. Article
  6. Mucin-Type O-GalNAc Glycosylation in Health and Disease.Advances in experimental medicine and biology · 2021
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Skin manifestations in CDG.Journal of inherited metabolic disease · 2014
    Review
  13. Mucin-type O-glycosylation during development.The Journal of biological chemistry · 2013
    Review
  14. Article
  15. Article
  16. Fibroblast growth factor 23: state of the field and future directions.Trends in endocrinology and metabolism: TEM · 2012
    Review
  17. Article
  18. Vitamin D safety and requirements.Archives of biochemistry and biophysics · 2012
    Review
  19. Article
  20. 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 2 institutions in 1 country.

Ilana ChefetzCenter for Translational Genetics, Rappaport Institute for Research in the Medical Sciences, Haifa, Israel.
Eli Sprecher
Technion – Israel Institute of Technology · ILTel Aviv Sourasky Medical Center · IL

Funding

Molecular Genetics of Familial Tumoral CalcinosisR01AR052627 · NIAMS · THOMAS JEFFERSON UNIVERSITY · PI UITTO, JOUNI · 2005 to 2009
$1.6M
NIAMS NIH HHS R01 AR052627
6 · The paper itself

Abstract

Familial tumoral calcinosis refers to a group of disorders inherited in an autosomal recessive fashion. Hyperphosphatemic tumoral calcinosis is characterized by increased re-absorption of phosphate through the renal proximal tubule, resulting in elevated phosphate concentration and deposition of calcified deposits in cutaneous and subcutaneous tissues, as well as, occasionally, in visceral organs. The disease was found to result from mutations in at least 3 genes: GALNT3, encoding a glycosyltransferase termed ppGalNacT3, FGF23 encoding a potent phosphaturic protein, and KL encoding Klotho. Recent data showed that ppGalNacT3 mediates O-glycosylation of FGF23, thereby allowing for its secretion and possibly protecting it from proteolysis-mediated inactivation. Klotho was found to serve as a co-receptor for FGF23, thereby integrating the genetic data into a single physiological system. The elucidation of the molecular basis of HFTC shed new light upon the mechanisms regulating phosphate homeostasis, suggesting innovative therapeutic strategies for the management of hyperphosphatemia in common acquired conditions such as chronic renal failure.

Indexed as

CalcinosisFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseGlycosylationHomeostasisHumansHyperphosphatemiaKlotho ProteinsN-AcetylgalactosaminyltransferasesPhosphatesPolypeptide N-acetylgalactosaminyltransferaseFGF23 protein, humanFibroblast Growth Factor-23Fibroblast Growth FactorsGlucuronidaseKlotho ProteinsN-AcetylgalactosaminyltransferasesPhosphatesPolypeptide N-acetylgalactosaminyltransferase

Identifiers

PMID19013236
PMCPMC3169301
OpenAlexW2114328476

What OpenQuestion holds

Textmetadata
LicenceTDM
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.