Evidence map›Paper›PMID 23707302›Full record

ReviewDNA repair2013

ATM-deficient human neural stem cells as an in vitro model system to study neurodegeneration.

Luigi Carlessi, Elena Fusar Poli, Lidia De Filippis, Domenico Delia

Open access · hybridAbstract readReview
In one paragraph

Review in DNA repair, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Stem cell models in ataxia-telangiectasia.Neural regeneration research · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Genome-wide pathway analysis in attention-deficit/hyperactivity disorder.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014
    Article
  9. Article
  10. 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

4 authors at 2 institutions in 1 country.

Luigi CarlessiDepartment of Experimental Oncology, Fondazione IRCCS Istituto Nazionale Tumori, Via Amadeo 42, 20133, Milan, Italy.
Elena Fusar Poli
Lidia De Filippis
Domenico Delia
Fondazione IRCCS Istituto Nazionale dei Tumori · ITUniversity of Milano-Bicocca · IT

Funding

Telethon GGP10066
6 · The paper itself

Abstract

Loss of ATM kinase, a transducer of the DNA damage response and redox sensor, causes the neurodegenerative disorder ataxia-telangiectasia (A-T). While a great deal of progress has been made in elucidating the ATM-dependent DNA damage response (DDR) network, a key challenge remains in understanding the selective susceptibility of the nervous system to faulty DDR. Several factors appear implicated in the neurodegenerative phenotype in A-T, but which of them plays a crucial role remains unclear, especially since mouse models of A-T do not fully mirror the respective human syndrome. Therefore, a number of human neural stem cell (hNSC) systems have been developed to get an insight into the molecular mechanisms of neurodegeneration as consequence of ATM inactivation. Here we review the hNSC systems developed by us an others to model A-T.

Indexed as

AnimalsAtaxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsCell DifferentiationDisease Models, AnimalDNA DamageHumansNervous SystemNeural Stem CellsNeurodegenerative DiseasesNeuronsOxidative StressAtaxia Telangiectasia Mutated ProteinsATMDNA damage responseHypoxiaiPS cellsNeural stem cellsNeurodegeneration

Identifiers

PMID23707302
PMCPMC3732388
OpenAlexW2023830476

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.