Evidence map›Paper›PMID 27105496›Full record

ArticleOncotarget2016

Gadd45b deficiency promotes premature senescence and skin aging.

Andrew Magimaidas, Priyanka Madireddi, Silvia Maifrede, Kaushiki Mukherjee, Barbara Hoffman, Dan A Liebermann

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. GADD45 in Stress Signaling, Cell Cycle Control, and Apoptosis.Advances in experimental medicine and biology · 2022
    Article
  7. Roles for GADD45 in Development and Cancer.Advances in experimental medicine and biology · 2022
    Review
  8. Gadd45 in DNA Demethylation and DNA Repair.Advances in experimental medicine and biology · 2022
    Article
  9. Gadd45 in Senescence.Advances in experimental medicine and biology · 2022
    Article
  10. Article
  11. Article
  12. Article
  13. 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

6 authors at 1 institution in 1 country.

Andrew MagimaidasFels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA, USA.
Priyanka MadireddiFels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA, USA.
Silvia MaifredeFels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA, USA.
Kaushiki MukherjeeFels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA, USA.
Barbara HoffmanFels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA, USA.
Dan A LiebermannFels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, PA, USA.
Temple University · US

Funding

Gadd 45 genes sensors of stress and tumor modulatorsR01CA122376 · NCI · TEMPLE UNIV OF THE COMMONWEALTH · PI LIEBERMANN, DAN A · 2007 to 2011
$1.6M
NCI NIH HHS R01 CA122376
6 · The paper itself

Abstract

The GADD45 family of proteins functions as stress sensors in response to various physiological and environmental stressors. Here we show that primary mouse embryo fibroblasts (MEFs) from Gadd45b null mice proliferate slowly, accumulate increased levels of DNA damage, and senesce prematurely. The impaired proliferation and increased senescence in Gadd45b null MEFs is partially reversed by culturing at physiological oxygen levels, indicating that Gadd45b deficiency leads to decreased ability to cope with oxidative stress. Interestingly, Gadd45b null MEFs arrest at the G2/M phase of cell cycle, in contrast to other senescent MEFs, which arrest at G1. FACS analysis of phospho-histone H3 staining showed that Gadd45b null MEFs are arrested in G2 phase rather than M phase. H2O2 and UV irradiation, known to increase oxidative stress, also triggered increased senescence in Gadd45b null MEFs compared to wild type MEFs. In vivo evidence for increased senescence in Gadd45b null mice includes the observation that embryos from Gadd45b null mice exhibit increased senescence staining compared to wild type embryos. Furthermore, it is shown that Gadd45b deficiency promotes senescence and aging phenotypes in mouse skin. Together, these results highlight a novel role for Gadd45b in stress-induced senescence and in tissue aging.

Indexed as

AnimalsAntigens, DifferentiationCell ProliferationCells, CulturedCellular SenescenceEmbryo, MammalianFibroblastsG2 Phase Cell Cycle CheckpointsGADD45 ProteinsHydrogen PeroxideMice, KnockoutOxidantsOxidative StressOxygenSkin AgingUltraviolet RaysAntigens, DifferentiationGadd45b protein, mouseGADD45 ProteinsHydrogen PeroxideOxidantsOxygencell cycle arrestDNA damageGadd45bGerotargetoxidative stresssenescence

Identifiers

PMID27105496
PMCPMC5053623
OpenAlexW2336503309

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.