Evidence map›Paper›PMID 21660944›Full record

ReviewJournal of cellular physiology2011

The p53 tumor suppressor protein regulates hematopoietic stem cell fate.

Takashi Asai, Yan Liu, Narae Bae, Stephen D Nimer

Abstract readReview
In one paragraph

Review in Journal of cellular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

60 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Pandora's Box of AML: HowBiomedicines · 2025
    Review
  3. Metabolomics of healthy hematopoietic stem cells and leukemic stem cells.Journal of clinical and translational research · 2025
    Article
  4. Article
  5. Hematopoietic stem cell metabolism within the bone marrow niche - insights and opportunities.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  6. Article
  7. Acute Erythroid Leukemia: From Molecular Biology to Clinical Outcomes.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Discrete Logic Modeling of Cell Signaling Pathways.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  19. Article
  20. Review
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.

Takashi AsaiSloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.
Yan Liu
Narae Bae
Stephen D Nimer
Memorial Sloan Kettering Cancer Center · US

Funding

FUNCTION OF MEF IN HEMATOPOIETIC CELLSR01DK052208 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI NIMER, STEPHEN D. · 1997 to 2011
$3.1M
Function of MEF in Hematopoietic CellsR56DK052208 · NIDDK · SLOAN-KETTERING INST CAN RESEARCH · PI NIMER, STEPHEN DAVID · 2007 to 2007
$500k
NIDDK NIH HHS DK52208NIDDK NIH HHS R01 DK052208NIDDK NIH HHS R56 DK052208
6 · The paper itself

Abstract

The p53 tumor suppressor protein is a key transcription factor that regulates several signaling pathways involved in the cell's response to stress. Through stress-induced activation, p53 accumulates and triggers the expression of target genes that protect the genetic integrity of all cells including hematopoietic stem cells (HSCs). These protective mechanisms include cell-cycle arrest, DNA repair, induction of apoptosis, or initiation of senescence. In addition to its function under stress conditions, p53 has important functions during steady-state hematopoiesis, regulating HSC quiescence and self-renewal. In addition, it appears that p53 levels affect HSC competition for the hematopoietic niche, with the less p53 activated HSCs preferentially surviving. The specific genes and precise mechanisms underlying p53's effects on normal HSCs are slowly being clarified. p53 also plays an important role in leukemia stem cell (LSC) behavior, with p53 loss affecting drug resistance and disease progression. Pharmacologic activation of p53 function could overcome the adverse impact of p53 inactivation in LSCs. Thus, understanding the p53 regulatory mechanisms active in HSCs and LSCs may promote the development of new therapeutic strategies that could eliminate the population of largely quiescent LSCs.

Indexed as

Cell LineageAnimalsCellular SenescenceHematopoietic Stem CellsHumansNeoplastic Stem CellsStress, PhysiologicalTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID21660944
PMCPMC3081536
OpenAlexW2111718423

What OpenQuestion holds

Textmetadata
LicenceTDM
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.