Evidence map›Paper›PMID 10791995›Full record

ArticleThe Journal of clinical investigation2000

Genes that modify the hemochromatosis phenotype in mice.

J E Levy, L K Montross, N C Andrews

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
13.6field-weighted citation impact, top 1% 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

68 citing papers in PubMed, 214 citations in OpenAlex.

  1. The neogenin-hemojuvelin axis in murine liver is crucial for hepcidin expression.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Article
  2. Article
  3. Review
  4. Revisiting hemochromatosis: geneticAnnals of translational medicine · 2021
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Oral nucleic acid therapy using multicompartmental delivery systems.Wiley interdisciplinary reviews. Nanomedicine and nanobiotechnology · 2018
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Epistasis in iron metabolism: complex interactions between Cp, Mon1a, and Slc40a1 loci and tissue iron in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2013
    Article
  20. Review

8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

J E LevyDivision of Hematology-Oncology, Children's Hospital, Boston, Massachusetts 02115, USA.
L K Montross
N C Andrews
Howard Hughes Medical Institute · USBrigham and Women's Hospital · US

Funding

REGULATION OF ERYTHROPOIESISR01HL051057 · NHLBI · DUKE UNIVERSITY · PI ANDREWS, NANCY CATHERINE · 1999 to 2007
$2.2M
NHLBI NIH HHS K08HLO30505NHLBI NIH HHS R01 HL051057NHLBI NIH HHS R01HL51057
6 · The paper itself

Abstract

Hereditary hemochromatosis (HH) is a prevalent human disease caused by a mutation in HFE, which encodes an atypical HLA class I protein involved in regulation of intestinal iron absorption. To gain insight into the pathogenesis of hemochromatosis, we have bred Hfe knockout mice to strains carrying other mutations that impair normal iron metabolism. Compound mutant mice lacking both Hfe and its interacting protein, beta-2 microglobulin (B2m), deposit more tissue iron than mice lacking Hfe only, suggesting that another B2m-interacting protein may be involved in iron regulation. Hfe knockout mice carrying mutations in the iron transporter DMT1 fail to load iron, indicating that hemochromatosis involves iron flux through DMT1. Similarly, compound mutants deficient in both Hfe and hephaestin (Heph) show less iron loading than do Hfe knockout mice, indicating that iron absorption in hemochromatosis involves the function of Heph as well. Finally, compound mutants lacking Hfe and the transferrin receptor accumulate more tissue iron than do mice lacking Hfe alone, consistent with the idea that interaction between these two proteins contributes to the control of normal iron absorption. In addition to providing insight into the pathogenesis of HH, our results suggest that each of these genes might be a candidate modifier of the human hemochromatosis phenotype.

Indexed as

Cation Transport ProteinsIron-Binding ProteinsAnimalsbeta 2-MicroglobulinCarrier ProteinsHemochromatosisHemochromatosis ProteinHistocompatibility Antigens Class IHLA AntigensHomeostasisIntestinal AbsorptionIron, DietaryLiverMembrane ProteinsMiceMice, Knockoutbeta 2-MicroglobulinCarrier ProteinsCation Transport ProteinsHemochromatosis ProteinHfe protein, mouseHistocompatibility Antigens Class IHLA AntigensIron-Binding ProteinsIron, DietaryMembrane ProteinsReceptors, TransferrinSolute Carrier Family 11, Member 2

Identifiers

PMID10791995
PMCPMC315447
OpenAlexW2161918511

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.