Evidence map›Paper›PMID 22332037›Full record

ReviewAdvances in nutrition (Bethesda, Md.)2011

Impact of copper limitation on expression and function of multicopper oxidases (ferroxidases).

Joseph R Prohaska

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Advances in nutrition (Bethesda, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
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  8. Observational
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  15. The biology of mammalian multi-copper ferroxidases.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2023
    Review
  16. Article
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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

1 author at 1 institution in 1 country.

Joseph R ProhaskaDepartment of Biochemistry and Molecular Biology, University of Minnesota Medical School, Duluth, MN 55812, USA. jprohask@d.umn.edu
University of Minnesota, Duluth · US

Funding

NUTRITIONAL COPPER STATUS AND THE NERVOUS SYSTEMR01HD039708 · NICHD · UNIVERSITY OF MINNESOTA DULUTH · PI PROHASKA, JOSEPH ROBERT · 2001 to 2010
$1.5M
NICHD NIH HHS HD039708NICHD NIH HHS R01 HD039708
6 · The paper itself

Abstract

Copper is an essential trace element whose recommended intake is met by most North American diets. However, incidence of new cases of secondary copper deficiency is rising due to complications of gastric bypass surgery and high zinc exposure. Patients frequently are ataxic and anemic. Anemia of copper deficiency was first described in the 19th century, but the underlying biochemistry remains unknown. Approximately one dozen cuproenzymes have been characterized in mammals. Four of these are referred to as multicopper oxidases (MCO) due to their copper binding geometries. They have iron oxidase activity (ferroxidase). These include the hepatic secreted protein ceruloplasmin representing ∼90% of plasma copper, a splice-variant of ceruloplasmin originally characterized in brain linked by glycosylphosphatidylinositol (GPI) to membranes, an intestinal enriched MCO named hephaestin, and newly described MCO in placenta called zyklopen. Limitation in available copper appears to limit function of the MCO group exhibited as impaired iron flux due to the copper requirement of MCO for their ferroxidase activity. Dietary copper deficiency is associated with lower levels of ceruloplasmin, GPI-ceruloplasmin, and hephaestin. Limitation of copper does not appear to limit synthesis of MCO but rather their stability and turnover. However, there appears to be a disconnect between limitation in MCO function and anemia, because humans and mice missing ceruloplasmin are not anemic despite hepatic iron overload and hypoferremia. Furthermore, anemic copper-deficient mammals are not improved by iron replacement. This suggests that the anemia of copper deficiency is not caused by iron limitation but rather impairment in iron utilization.

Indexed as

Anemia, HypochromicAnimalsCeruloplasminCopperGPI-Linked ProteinsHumansMiceRatsCeruloplasminCopperGPI-Linked Proteins

Identifiers

PMID22332037
PMCPMC3065751
OpenAlexW2133727381

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.