Evidence map›Paper›PMID 22460705›Full record

ArticleAmerican journal of hematology2012

Transgenic HFE-dependent induction of hepcidin in mice does not require transferrin receptor-2.

Paul J Schmidt, Mark D Fleming

Open access · bronzeAbstract read
In one paragraph

Article in American journal of hematology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Coordination of iron homeostasis by bone morphogenetic proteins: Current understanding and unanswered questions.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Iron as a Therapeutic Target inPharmaceuticals (Basel, Switzerland) · 2018
    Review
  10. Haemochromatosis.Nature reviews. Disease primers · 2018
    Review
  11. Article
  12. Iron homeostasis: An anthropocentric perspective.The Journal of biological chemistry · 2017
    Review
  13. Review
  14. Review
  15. Hfe and Hjv exhibit overlapping functions for iron signaling to hepcidin.Journal of molecular medicine (Berlin, Germany) · 2015
    Article
  16. Review
  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

2 authors at 2 institutions in 1 country.

Paul J SchmidtDepartment of Pathology, Children's Hospital Boston and Harvard Medical School, 320 Longwood Ave., Boston, MA 02115, USA. pschmidt@enders.tch.harvard.edu
Mark D Fleming
Boston Children's Hospital · USHarvard University · US

Funding

CORE--ZEBRAFISHP30DK049216 · NIDDK · CHILDREN'S HOSPITAL BOSTON · PI ORKIN, STUART H · 1999 to 2015
$14.3M
Metalloreductases in MedicineR01DK080011 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI FLEMING, MARK D · 2007 to 2010
$1.3M
Study of the HFE Transferrin Receptor interaction in mammalian iron homeostasisK01DK074410 · NIDDK · BOSTON CHILDREN'S HOSPITAL · PI SCHMIDT, PAUL J · 2006 to 2010
$646k
NIDDK NIH HHS K01 DK074410NIDDK NIH HHS P30 DK049216NIDDK NIH HHS R01 DK080011
6 · The paper itself

Abstract

Hereditary hemochomatosis (HH) is caused by mutations in several genes, including HFE and transferrin receptor-2 (TFR2). Loss of either protein decreases expression of the iron regulatory hormone hepcidin by the liver, leading to inappropriately high iron uptake from the diet, and resulting in systemic iron overload. In tissue culture, overexpressed HFE and TFR2 physically interact. Hepatocellular overexpression of Hfe in vivo increases hepcidin expression, despite an associated decrease in Tfr2. On this basis, we hypothesized that Tfr2 would not be required for Hfe-dependent up-regulation of hepcidin. We show that hepatocellular overexpression of Hfe in Tfr2(Y245X/Y245X) mice leads to hepcidin induction eventuating in iron deficiency and a hypochromic, microcytic anemia. Furthermore, coimmunoprecipitation studies using liver lysates did not provide evidence for physical interaction between Hfe and Tfr2 in vivo. In conclusion, we demonstrate that Tfr2 is not essential for Hfe-mediated induction of hepcidin expression, supporting the possibility that TFR2 may regulate iron metabolism in an HFE-independent manner.

Indexed as

Anemia, HypochromicAnimalsAntimicrobial Cationic Peptidesbeta 2-MicroglobulinCell MembraneGene Expression RegulationGenes, SyntheticHemochromatosis ProteinHepcidinsHistocompatibility Antigens Class IIronLiverMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutAntimicrobial Cationic Peptidesbeta 2-MicroglobulinHamp protein, mouseHemochromatosis ProteinHepcidinsHfe protein, mouseHistocompatibility Antigens Class IIronMembrane ProteinsPrealbuminReceptors, TransferrinRecombinant Fusion ProteinsTFR2 protein, mouseTfrc protein, mouse

Identifiers

PMID22460705
PMCPMC3386558
OpenAlexW2006204635

What OpenQuestion holds

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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.