Evidence map›Paper›PMID 22776820›Full record

ArticleBlood2012

Necdin, a p53 target gene, regulates the quiescence and response to genotoxic stress of hematopoietic stem/progenitor cells.

Takashi Asai, Yan Liu, Silvana Di Giandomenico, Narae Bae, Delphine Ndiaye-Lobry, Anthony Deblasio, Silvia Menendez, Yevgeniy Antipin, Boris Reva, Rachel Wevrick and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.3field-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

45 citing papers in PubMed, 70 citations in OpenAlex.

  1. Haematologica · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Clonal hematopoiesis and bone marrow inflammation.Translational research : the journal of laboratory and clinical medicine · 2023
    Review
  11. TP53-Mutated Myelodysplasia and Acute Myeloid Leukemia.Mediterranean journal of hematology and infectious diseases · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Molecular regulation of hematopoietic stem cell quiescence.Cellular and molecular life sciences : CMLS · 2022
    Review
  16. Review
  17. Article
  18. 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

11 authors at 3 institutions in 2 countries.

Takashi AsaiMolecular Pharmacology and Chemistry Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY, USA.
Yan Liu
Silvana Di Giandomenico
Narae Bae
Delphine Ndiaye-Lobry
Anthony Deblasio
Silvia Menendez
Yevgeniy Antipin
Boris Reva
Rachel Wevrick
Stephen D Nimer
Memorial Sloan Kettering Cancer Center · USUniversity of Alberta · CAUniversity of Miami · 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 R01 DK052208NIDDK NIH HHS R01 DK52208NIDDK NIH HHS R56 DK052208
6 · The paper itself

Abstract

We recently defined a critical role for p53 in regulating the quiescence of adult hematopoietic stem cells (HSCs) and identified necdin as a candidate p53 target gene. Necdin is a growth-suppressing protein and the gene encoding it is one of several that are deleted in patients with Prader-Willi syndrome. To define the intrinsic role of necdin in adult hematopoiesis, in the present study, we transplanted necdin-null fetal liver cells into lethally irradiated recipients. We show that necdin-null adult HSCs are less quiescent and more proliferative than normal HSCs, demonstrating the similar role of necdin and p53 in promoting HSC quiescence during steady-state conditions. However, wild-type recipients repopulated with necdin-null hematopoietic stem/progenitor cells show enhanced sensitivity to irradiation and chemotherapy, with increased p53-dependent apoptosis, myelosuppression, and mortality. Necdin controls the HSC response to genotoxic stress via both cell-cycle-dependent and cell-cycle-independent mechanisms, with the latter occurring in a Gas2L3-dependent manner. We conclude that necdin functions as a molecular switch in adult hematopoiesis, acting in a p53-like manner to promote HSC quiescence in the steady state, but suppressing p53-dependent apoptosis in response to genotoxic stress.

Indexed as

DNA DamageHematopoiesisAnimalsApoptosisCell ProliferationCells, CulturedDrug TherapyGene DeletionGenes, p53Hematopoietic Stem CellsLiverMiceMice, Inbred C57BLNerve Tissue ProteinsNuclear ProteinsTumor Suppressor Protein p53necdinNerve Tissue ProteinsNuclear ProteinsTumor Suppressor Protein p53

Identifiers

PMID22776820
PMCPMC3429304
OpenAlexW2026257211

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.