Evidence map›Paper›PMID 28931909›Full record

ArticleScientific reports2017

Organ-specific regulation of ATP7A abundance is coordinated with systemic copper homeostasis.

Haarin Chun, Tracy Catterton, Heejeong Kim, Jaekwon Lee, Byung-Eun Kim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. 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
1.9field-weighted citation impact, top 14% 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, 39 citations in OpenAlex.

  1. Balancing cellular copper levels via the post-translational regulation of copper transport.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Secretion and uptake of copper via a small copper carrier in blood fluid.Metallomics : integrated biometal science · 2022
    Article
  12. Oral Elesclomol Treatment Alleviates Copper Deficiency in Animal Models.Frontiers in cell and developmental biology · 2022
    Article
  13. Article
  14. Review
  15. COMMD1 upregulation is involved in copper efflux from ischemic hearts.Experimental biology and medicine (Maywood, N.J.) · 2021
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Changes in mammalian copper homeostasis during microbial infection.Metallomics : integrated biometal science · 2020
    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

5 authors at 2 institutions in 1 country.

Haarin ChunDepartment of Animal and Avian Sciences, University of Maryland, College Park, MD 20742, USA.
Tracy CattertonDepartment of Animal and Avian Sciences, University of Maryland, College Park, MD 20742, USA.
Heejeong KimDepartment of Biochemistry and Redox Biology Center, University of Nebraska, Lincoln, NE 68516, USA.
Jaekwon LeeDepartment of Biochemistry and Redox Biology Center, University of Nebraska, Lincoln, NE 68516, USA.
Byung-Eun KimDepartment of Animal and Avian Sciences, University of Maryland, College Park, MD 20742, USA. bekim@umd.edu.
University of Maryland, College Park · USUniversity of Nebraska–Lincoln · US

Funding

Redox Biology CenterP30GM103335 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI BECKER, DONALD F · 2012 to 2016
$4.3M
Mechanistic insights into homeostatic copper acquistionR01DK079209 · NIDDK · UNIVERSITY OF NEBRASKA LINCOLN · PI LEE, JAEKWON · 2007 to 2014
$1.9M
NIDDK NIH HHS R01 DK079209NIGMS NIH HHS P30 GM103335
6 · The paper itself

Abstract

Copper (Cu) is an essential cofactor for various enzymatic activities including mitochondrial electron transport, iron mobilization, and peptide hormone maturation. Consequently, Cu dysregulation is associated with fatal neonatal disease, liver and cardiac dysfunction, and anemia. While the Cu transporter ATP7A plays a major role in both intestinal Cu mobilization to the periphery and prevention of Cu over-accumulation, it is unclear how regulation of ATP7A contributes to Cu homeostasis in response to systemic Cu fluctuation. Here we show, using Cu-deficient mouse models, that steady-state levels of ATP7A are lower in peripheral tissues (including the heart, spleen, and liver) under Cu deficiency and that subcutaneous administration of Cu to these animals restore normal ATP7A levels in these tissues. Strikingly, ATP7A in the intestine is regulated in the opposite manner - low systemic Cu increases ATP7A while subcutaneous Cu administration decreases ATP7A suggesting that intestine-specific non-autonomous regulation of ATP7A abundance may serve as a key homeostatic control for Cu export into the circulation. Our results support a systemic model for how a single transporter can be inversely regulated in a tissue-specific manner to maintain organismal Cu homeostasis.

Indexed as

HomeostasisOrgan SpecificityAnimalsCation Transport ProteinsCells, CulturedCopperCopper Transporter 1Copper-Transporting ATPasesEpithelial CellsHumansIntestinal MucosaLiverMice, Inbred C57BLMice, KnockoutPhenanthrolinesRatsbathocuproine sulfonateCation Transport ProteinsCopperCopper Transporter 1Copper-Transporting ATPasesPhenanthrolinesSlc31a1 protein, mouse

Identifiers

PMID28931909
PMCPMC5607234
OpenAlexW2754938564

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.