Evidence map›Paper›PMID 23187127›Full record

ArticleThe Journal of clinical investigation2012

The mitochondrial heme exporter FLVCR1b mediates erythroid differentiation.

Deborah Chiabrando, Samuele Marro, Sonia Mercurio, Carlotta Giorgi, Sara Petrillo, Francesca Vinchi, Veronica Fiorito, Sharmila Fagoonee, Annalisa Camporeale, Emilia Turco and 5 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 130 papers.

0numbers the graph read from it
0cells of the map it votes in
130citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

130 citing papers in PubMed, 193 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Light-Inducible Bispecific DNAzymes Reveal Mitochondrial FeAngewandte Chemie (International ed. in English) · 2026
    Article
  7. More than a ring: the emerging role of heme in angiogenesis.Cell communication and signaling : CCS · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Key roles of GAPDH, Hsp90, and NO in heme trafficking.Journal of inorganic biochemistry · 2026
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Mechanisms of heme transport in the mitochondria.Biochemical Society transactions · 2025
    Review
  19. Heme metabolism mediates RANKL-induced osteoclastogenesis via mitochondrial oxidative phosphorylation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025
    Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 2 countries.

Deborah ChiabrandoMolecular Biotechnology Centre, Department of Genetics, Biology and Biochemistry, University of Torino, Torino, Italy.
Samuele Marro
Sonia Mercurio
Carlotta Giorgi
Sara Petrillo
Francesca Vinchi
Veronica Fiorito
Sharmila Fagoonee
Annalisa Camporeale
Emilia Turco
Giorgio R Merlo
Lorenzo Silengo
Fiorella Altruda
Paolo Pinton
Emanuela Tolosano
University of Turin · ITUniversity of Ferrara · IT

Funding

Telethon GGP09128Telethon GGP11139
6 · The paper itself

Abstract

Feline leukemia virus subgroup C receptor 1 (FLVCR1) is a cell membrane heme exporter that maintains the balance between heme levels and globin synthesis in erythroid precursors. It was previously shown that Flvcr1-null mice died in utero due to a failure of erythropoiesis. Here, we identify Flvcr1b, a mitochondrial Flvcr1 isoform that promotes heme efflux into the cytoplasm. Flvcr1b overexpression promoted heme synthesis and in vitro erythroid differentiation, whereas silencing of Flvcr1b caused mitochondrial heme accumulation and termination of erythroid differentiation. Furthermore, mice lacking the plasma membrane isoform (Flvcr1a) but expressing Flvcr1b had normal erythropoiesis, but exhibited hemorrhages, edema, and skeletal abnormalities. Thus, FLVCR1b regulates erythropoiesis by controlling mitochondrial heme efflux, whereas FLVCR1a expression is required to prevent hemorrhages and edema. The aberrant expression of Flvcr1 isoforms may play a role in the pathogenesis of disorders characterized by an imbalance between heme and globin synthesis.

Indexed as

Cell DifferentiationAbnormalities, MultipleAnimalsBone Diseases, DevelopmentalBrainEdemaErythrocytesErythropoiesisExonsGene ExpressionGene Knockdown TechniquesHEK293 CellsHeLa CellsHemeHemorrhageHumansFLVCR1 protein, humanHemeMembrane Transport ProteinsMitochondrial ProteinsProtein IsoformsReceptors, Virus

Identifiers

PMID23187127
PMCPMC3533534
OpenAlexW2022334625

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.