Evidence map›Paper›PMID 24159174›Full record

ArticleBlood2014

Tropomodulin3-null mice are embryonic lethal with anemia due to impaired erythroid terminal differentiation in the fetal liver.

Zhenhua Sui, Roberta B Nowak, Andrea Bacconi, Nancy E Kim, Hui Liu, Jie Li, Amittha Wickrema, Xiu-li An, Velia M Fowler

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 8% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Genetic abnormalities and pregnancy loss.Seminars in perinatology · 2019
    Pooled it
  2. Article
  3. Macrophages in Hematopoiesis and Related Blood Diseases.Genomics, proteomics & bioinformatics · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Fine-Tuning of Cholesterol Homeostasis Controls Erythroid Differentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Zhenhua SuiThe Scripps Research Institute, La Jolla, CA;
Roberta B Nowak
Andrea Bacconi
Nancy E Kim
Hui Liu
Jie Li
Amittha Wickrema
Xiu-li An
Velia M Fowler
Scripps Research Institute · USNew York Blood Center · USUniversity of Chicago · US

Funding

YEAST MEMBRANE CYTOSKELETONP01DK032094 · NIDDK · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI NARLA, MOHANDAS · 1987 to 2021
$26.7M
Capping Actin Growth in Erythroid and Nonerythroid CellsR01HL083464 · NHLBI · UNIVERSITY OF DELAWARE · PI FOWLER, VELIA M · 2006 to 2019
$7.1M
RED CELL DEFORMABILITY IN VITRO AND SURVIVAL IN VIVOR37DK026263 · NIDDK · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI NARLA, MOHANDAS · 1995 to 2017
$4.5M
RED CELL DEFORMABILITY IN VITRO AND SURVIVAL IN VIVOR01DK026263 · NIDDK · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI NARLA, MOHANDAS · 1986 to 2007
$1.6M
NHLBI NIH HHS R01 HL083464NHLBI NIH HHS R01-HL083464NIDDK NIH HHS DK26263NIDDK NIH HHS DK32094NIDDK NIH HHS P01 DK032094NIDDK NIH HHS R01 DK026263NIDDK NIH HHS R37 DK026263
6 · The paper itself

Abstract

Tropomodulin (Tmod) is a protein that binds and caps the pointed ends of actin filaments in erythroid and nonerythoid cell types. Targeted deletion of mouse tropomodulin3 (Tmod3) leads to embryonic lethality at E14.5-E18.5, with anemia due to defects in definitive erythropoiesis in the fetal liver. Erythroid burst-forming unit and colony-forming unit numbers are greatly reduced, indicating defects in progenitor populations. Flow cytometry of fetal liver erythroblasts shows that late-stage populations are also decreased, including reduced percentages of enucleated cells. Annexin V staining indicates increased apoptosis of Tmod3(-/-) erythroblasts, and cell-cycle analysis reveals that there are more Ter119(hi) cells in S-phase in Tmod3(-/-) embryos. Notably, enucleating Tmod3(-/-) erythroblasts are still in the process of proliferation, suggesting impaired cell-cycle exit during terminal differentiation. Tmod3(-/-) late erythroblasts often exhibit multilobular nuclear morphologies and aberrant F-actin assembly during enucleation. Furthermore, native erythroblastic island formation was impaired in Tmod3(-/-) fetal livers, with Tmod3 required in both erythroblasts and macrophages. In conclusion, disruption of Tmod3 leads to impaired definitive erythropoiesis due to reduced progenitors, impaired erythroblastic island formation, and defective erythroblast cell-cycle progression and enucleation. Tmod3-mediated actin remodeling may be required for erythroblast-macrophage adhesion, coordination of cell cycle with differentiation, and F-actin assembly and remodeling during erythroblast enucleation.

Indexed as

Gene DeletionAnimalsApoptosisCell CycleErythroblastsErythroid Precursor CellsErythropoiesisFemaleGene Expression Regulation, DevelopmentalLiverMaleMiceMice, KnockoutTropomodulinTmod1 protein, mouseTmod3 protein, mouseTropomodulin

Identifiers

PMID24159174
PMCPMC3907761
OpenAlexW2090390052

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.