Evidence map›Paper›PMID 24021674›Full record

ArticleBlood2013

FLVCR is necessary for erythroid maturation, may contribute to platelet maturation, but is dispensable for normal hematopoietic stem cell function.

John C H Byon, Jing Chen, Raymond T Doty, Janis L Abkowitz

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

16 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Unearthing FLVCR1a: tracing the path to a vital cellular transporter.Cellular and molecular life sciences : CMLS · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. GAPDH is involved in the heme-maturation of myoglobin and hemoglobin.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. Targeting iron metabolism in drug discovery and delivery.Nature reviews. Drug discovery · 2017
    Review
  14. Review
  15. Article
  16. 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

4 authors at 1 institution in 1 country.

John C H ByonDivision of Hematology, Department of Medicine, University of Washington, Seattle, WA.
Jing Chen
Raymond T Doty
Janis L Abkowitz
University of Washington · US

Funding

Physiology of feline leukemia virus C receptor, FLVCRR01HL031823 · NHLBI · UNIVERSITY OF WASHINGTON · PI ABKOWITZ, JANIS L · 1985 to 2024
$9.1M
Career Development in Clinical Hematology ResearchK12HL087165 · NHLBI · UNIVERSITY OF WASHINGTON · PI ABKOWITZ, JANIS L · 2006 to 2016
$4.0M
Heme trafficking and its impact on systemic iron homeostasisR01DK085146 · NIDDK · UNIVERSITY OF WASHINGTON · PI ABKOWITZ, JANIS L · 2011 to 2014
$1.4M
NHLBI NIH HHS K12 HL087165NHLBI NIH HHS R01 HL031823NIDDK NIH HHS R01 DK085146NIDDK NIH HHS R01DK085146
6 · The paper itself

Abstract

Heme is a pleiotropic molecule that is important for oxygen and oxidative metabolism, most notably as the prosthetic group of hemoglobin and cytochromes. Because excess free intracellular heme is toxic, organisms have developed mechanisms to tightly regulate its concentration. One mechanism is through active heme export by the group C feline leukemia virus receptor (FLVCR). Previously, we have shown that FLVCR is necessary for embryonic and postnatal erythropoiesis. However, FLVCR is also expressed in numerous other tissues, including hematopoietic stem cells (HSCs). To explore a possible role for FLVCR in HSC function, we performed serial, competitive repopulation transplant experiments using FLVCR-deleted and control bone marrow cells, along with wild-type competitor cells. Loss of FLVCR did not impact HSC function under steady-state or myelotoxic stress conditions (such as arsenic or radiation exposure), nor did FLVCR deletion result in alterations in the various progenitor compartments. However, even when 95% of the donor bone marrow cells lacked FLVCR, all red cells in recipient mice were wild type. This is due to the increased apoptosis of FLVCR-deleted proerythroblasts. Also, remarkably, loss of FLVCR increased megakaryocyte ploidy. Together, these findings show FLVCR is redundant in stem cells but has critical and contrasting stage-specific roles in discrete hematopoietic lineages.

Indexed as

Gene Expression RegulationAnimalsApoptosisBlood PlateletsCell LineageErythroblastsFemaleGene DeletionHematopoietic Stem CellsHemeMegakaryocytesMembrane Transport ProteinsMiceMice, Inbred C57BLMice, TransgenicOxidative StressFlvcr1 protein, mouseHemeMembrane Transport ProteinsReceptors, Virus

Identifiers

PMID24021674
PMCPMC3799002
OpenAlexW2040993335

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.