Evidence map›Paper›PMID 18397889›Full record

ArticleThe Journal of biological chemistry2008

Tumor suppressor protein p53 regulates megakaryocytic polyploidization and apoptosis.

Peter G Fuhrken, Pani A Apostolidis, Stephan Lindsey, William M Miller, Eleftherios T Papoutsakis

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

  1. Unraveling the role ofHemaSphere · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Trp53 regulates platelets in bone marrow via the PI3K pathway.Experimental and therapeutic medicine · 2020
    Article
  6. Article
  7. Induction of differentiation of human stem cellsWorld journal of stem cells · 2019
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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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

5 authors at 3 institutions in 1 country.

Peter G FuhrkenDepartment of Chemical and Biological Engineering, Northwestern University, Evanston, Illinois 60208, USA.
Pani A Apostolidis
Stephan Lindsey
William M Miller
Eleftherios T Papoutsakis
Biotechnology Institute · USNorthwestern University · USUniversity of Delaware · US

Funding

PO2 AND PH AS POTENT MODULATORS OF HEMATOPOIESISR01HL048276 · NHLBI · NORTHWESTERN UNIVERSITY · PI PAPOUTSAKIS, ELEFTHERIOS T · 1993 to 2007
$2.0M
NHLBI NIH HHS HL48276NHLBI NIH HHS R01 HL048276
6 · The paper itself

Abstract

The molecular mechanisms underlying differentiation of hematopoietic stem cells into megakaryocytes are poorly understood. Tumor suppressor protein p53 can act as a transcription factor affecting both cell cycle control and apoptosis, and we have previously shown that p53 is activated during terminal megakaryocytic (Mk) differentiation of the CHRF-288-11 (CHRF) cell line. Here, we use RNA interference to reduce p53 expression in CHRF cells and show that reduced p53 activity leads to a greater fraction of polyploid cells, higher mean and maximum ploidy, accelerated DNA synthesis, and delayed apoptosis and cell death upon phorbol 12-myristate 13-acetate-induced Mk differentiation. In contrast, reduced p53 expression did not affect the ploidy or DNA synthesis of CHRF cells in the absence of phorbol 12-myristate 13-acetate stimulation. Furthermore, primary Mk cells from cultures initiated with p53-null mouse bone marrow mononuclear cells displayed higher ploidy compared with wild-type controls. Quantitative reverse transcription-PCR analysis of p53-knockdown CHRF cells, compared with the "scrambled" control CHRF cells, revealed that six known transcriptional targets of p53 (BBC3, BAX, TP53I3, TP53INP1, MDM2, and P21) were down-regulated, whereas BCL2 expression, which is known to be negatively affected by p53, was up-regulated. These studies show that the functional role of the intrinsic activation of p53 during Mk differentiation is to control polyploidization and the transition to endomitosis by impeding cell cycling and promoting apoptosis.

Indexed as

PloidiesAnimalsApoptosisCarcinogensCell CycleCell DifferentiationCell LineDNADown-RegulationHumansMaleMegakaryocytesMiceMice, KnockoutTetradecanoylphorbol AcetateTumor Suppressor Protein p53CarcinogensDNATetradecanoylphorbol AcetateTumor Suppressor Protein p53

Identifiers

PMID18397889
PMCPMC2414295
OpenAlexW2007474198

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.