Evidence map›Paper›PMID 21068437›Full record

ArticleBlood2011

Haploinsufficiency for ribosomal protein genes causes selective activation of p53 in human erythroid progenitor cells.

Shilpee Dutt, Anupama Narla, Katherine Lin, Ann Mullally, Nirmalee Abayasekara, Christine Megerdichian, Frederick H Wilson, Treeve Currie, Arati Khanna-Gupta, Nancy Berliner and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 239 papers.

0numbers the graph read from it
0cells of the map it votes in
239citing papers in PubMed
14.2field-weighted citation impact, top 1% 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

239 citing papers in PubMed, 395 citations in OpenAlex.

  1. Trial
  2. Article
  3. Genetic influences on haematopoiesis.Nature reviews. Genetics · 2026
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  8. Unraveling the role ofHemaSphere · 2026
    Review
  9. Review
  10. HemaSphere · 2026
    Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Functional Characterization and Heterogeneity Analysis of Ribosomal Proteins in Mouse Preimplantation Embryos.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  19. Mechanisms of ribosomopathy and phase separation-related ribosomopathy.Journal of Zhejiang University. Science. B · 2025
    Review
  20. Review

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

Shilpee DuttDivision of Hematology, Brigham and Women's Hospital, Boston, MA, USA.
Anupama Narla
Katherine Lin
Ann Mullally
Nirmalee Abayasekara
Christine Megerdichian
Frederick H Wilson
Treeve Currie
Arati Khanna-Gupta
Nancy Berliner
Jeffery L Kutok
Benjamin L Ebert
Brigham and Women's Hospital · USBoston Children's Museum · USDana-Farber Cancer Institute · US

Funding

Tyrosine Kinases, Serine-Threonine Kinases,&Phosophatases in PathogenesisP01CA108631 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ESTEY, ELIHU · 2005 to 2009
$9.7M
Functional Genomic Dissection of Refractory AnemiaR01HL082945 · NHLBI · DANA-FARBER CANCER INSTITUTE · PI EBERT, BENJAMIN LEVINE · 2005 to 2022
$6.8M
NCI NIH HHS P01 CA108631NHLBI NIH HHS 5R01 HL082945NHLBI NIH HHS R01 HL082945Wellcome Trust
6 · The paper itself

Abstract

Haploinsufficiency for ribosomal protein genes has been implicated in the pathophysiology of Diamond-Blackfan anemia (DBA) and the 5q-syndrome, a subtype of myelodysplastic syndrome. The p53 pathway is activated by ribosome dysfunction, but the molecular basis for selective impairment of the erythroid lineage in disorders of ribosome function has not been determined. We found that p53 accumulates selectively in the erythroid lineage in primary human hematopoietic progenitor cells after expression of shRNAs targeting RPS14, the ribosomal protein gene deleted in the 5q-syndrome, or RPS19, the most commonly mutated gene in DBA. Induction of p53 led to lineage-specific accumulation of p21 and consequent cell cycle arrest in erythroid progenitor cells. Pharmacologic inhibition of p53 rescued the erythroid defect, whereas nutlin-3, a compound that activates p53 through inhibition of HDM2, selectively impaired erythropoiesis. In bone marrow biopsies from patients with DBA or del(5q) myelodysplastic syndrome, we found an accumulation of nuclear p53 staining in erythroid progenitor cells that was not present in control samples. Our findings indicate that the erythroid lineage has a low threshold for the induction of p53, providing a basis for the failure of erythropoiesis in the 5q-syndrome, DBA, and perhaps other bone marrow failure syndromes.

Indexed as

Anemia, Diamond-BlackfanAnemia, MacrocyticAnimalsBenzothiazolesCell CycleCell LineageCell NucleolusChromosome DeletionChromosomes, Human, Pair 5Cyclin-Dependent Kinase Inhibitor p21Erythroid Precursor CellsHaploinsufficiencyHematopoiesisHumansImidazolesMiceBenzothiazolesCyclin-Dependent Kinase Inhibitor p21ImidazolesMDM2 protein, humannutlin 3pifithrinPiperazinesProto-Oncogene Proteins c-mdm2ribosomal protein L11Ribosomal Proteinsribosomal protein S14ribosomal protein S19RNA, Small InterferingTolueneTumor Suppressor Protein p53

Identifiers

PMID21068437
PMCPMC3062351
OpenAlexW2133832061

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.