Evidence map›Paper›PMID 25150276›Full record

ArticleBiology open2014

Conditional inactivation of PDCD2 induces p53 activation and cell cycle arrest.

Celine J Granier, Wei Wang, Tiffany Tsang, Ruth Steward, Hatem E Sabaawy, Mantu Bhaumik, Arnold B Rabson

Abstract read
In one paragraph

Article in Biology open, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Frontiers in genetics · 2019
    Review
  7. Article
  8. Article
  9. Article
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

7 authors.

Celine J GranierChild Health Institute of New Jersey, Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ 08901, USA rabsonab@rwjms.rutgers.edu graniecj@rwjms.rutgers.edu.
Wei WangSequencing and Microarray Core Facility, Lewis-Sigler Institute for Integrative Genetics, Princeton University, Princeton, NJ 08854, USA.
Tiffany TsangChild Health Institute of New Jersey, Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ 08901, USA.
Ruth StewardWaksman Institute and Department of Molecular Biology, Rutgers University, Piscataway, NJ 08854, USA.
Hatem E SabaawyRutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ 08903, USA.
Mantu BhaumikChild Health Institute of New Jersey, Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ 08901, USA Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ 08903, USA.
Arnold B RabsonChild Health Institute of New Jersey, Robert Wood Johnson Medical School, Rutgers University, New Brunswick, NJ 08901, USA Rutgers Cancer Institute of New Jersey, Rutgers University, New Brunswick, NJ 08903, USA rabsonab@rwjms.rutgers.edu graniecj@rwjms.rutgers.edu.

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Chang S Chan · 1997 to 2026
$94.5M
NCI NIH HHS P30 CA072720
6 · The paper itself

Abstract

PDCD2 (programmed cell death domain 2) is a highly conserved, zinc finger MYND domain-containing protein essential for normal development in the fly, zebrafish and mouse. The molecular functions and cellular activities of PDCD2 remain unclear. In order to better understand the functions of PDCD2 in mammalian development, we have examined PDCD2 activity in mouse blastocyst embryos, as well as in mouse embryonic stem cells (ESCs) and embryonic fibroblasts (MEFs). We have studied mice bearing a targeted PDCD2 locus functioning as a null allele through a splicing gene trap, or as a conditional knockout, by deletion of exon2 containing the MYND domain. Tamoxifen-induced knockout of PDCD2 in MEFs, as well as in ESCs, leads to defects in progression from the G1 to the S phase of cell cycle, associated with increased levels of p53 protein and p53 target genes. G1 prolongation in ESCs was not associated with induction of differentiation. Loss of entry into S phase of the cell cycle and marked induction of nuclear p53 were also observed in PDCD2 knockout blastocysts. These results demonstrate a unique role for PDCD2 in regulating the cell cycle and p53 activation during early embryonic development of the mouse.

Indexed as

Cell cycleESCsMouse embryop53PDCD2Proliferation

Identifiers

PMID25150276
PMCPMC4163659

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Registered trials

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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.