Evidence map›Paper›PMID 21979466›Full record

ArticleCell death and differentiation2012

Terminally differentiated astrocytes lack DNA damage response signaling and are radioresistant but retain DNA repair proficiency.

L Schneider, M Fumagalli, F d'Adda di Fagagna

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

43 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Phosphorylation and DNA damage resolution coordinate SOX2-mediated reprogramming in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

3 authors at 1 institution in 1 country.

L SchneiderIFOM Foundation - The FIRC Institute of Molecular Oncology Foundation, Via Adamello 16, 20139 Milan, Italy. leonid.schneider@ifom-ieo-campus.it
M Fumagalli
F d'Adda di Fagagna
FIRC Institute of Molecular Oncology · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The impact and consequences of damage generation into genomic DNA, especially in the form of DNA double-strand breaks, and of the DNA-damage response (DDR) pathways that are promptly activated, have been elucidated in great detail. Most of this research, however, has been performed on proliferating, often cancerous, cell lines. In a mammalian body, the majority of cells are terminally differentiated (TD), and derives from a small pool of self-renewing somatic stem cells. Here, we comparatively studied DDR signaling and radiosensitivity in neural stem cells (NSC) and their TD-descendants, astrocytes - the predominant cells in the mammalian brain. Astrocytes have important roles in brain physiology, development and plasticity. We discovered that NSC activate canonical DDR upon exposure to ionizing radiation. Strikingly, astrocytes proved radioresistant, lacked functional DDR signaling, with key DDR genes such as ATM being repressed at the transcriptional level. Nevertheless, astrocytes retain the expression of non-homologous end-joining (NHEJ) genes and indeed they are DNA repair proficient. Unlike in NSC, in astrocytes DNA-PK seems to be the PI3K-like protein kinase responsible for γH2AX signal generation upon DNA damage. We also demonstrate the lack of functional DDR signaling activation in vivo in astrocytes of irradiated adult mouse brains, although adjacent neurons activate the DDR.

Indexed as

Cell DifferentiationAnimalsAstrocytesAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell LineDNA-Activated Protein KinaseDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA RepairGamma RaysMiceNeural Stem CellsNeuronsNuclear ProteinsPhosphatidylinositol 3-KinasesAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCell Cycle ProteinsDNA-Activated Protein KinaseDNA-Binding ProteinsNuclear ProteinsPhosphatidylinositol 3-KinasesPrkdc protein, mouseProtein Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID21979466
PMCPMC3307974
OpenAlexW2000399168

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.