Evidence map›Paper›PMID 35153719›Full record

ArticleFrontiers in aging neuroscience2021

The Essential DNA Damage Response Complex MRN Is Dispensable for the Survival and Function of Purkinje Neurons.

Mingmei Ding, Xiaobing Qing, Guangyu Zhang, Carolin Baade-Büttner, Ralph Gruber, Haizhen Lu, David O Ferguson, Christian Geis, Zhao-Qi Wang, Zhong-Wei Zhou

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 43% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
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

10 authors at 6 institutions in 3 countries.

Mingmei DingSchool of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.
Xiaobing QingLeibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.
Guangyu ZhangLeibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.
Carolin Baade-BüttnerSection of Translational Neuroimmunology, Department of Neurology, Jena University Hospital, Jena, Germany.
Ralph GruberLeibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.
Haizhen LuDepartment of Pathology and Resident Training Base, National Cancer Center/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
David O FergusonDepartment of Pathology and Comprehensive Cancer Center, University of Michigan Medical School, Ann Arbor, MI, United States.
Christian GeisSection of Translational Neuroimmunology, Department of Neurology, Jena University Hospital, Jena, Germany.
Zhao-Qi WangLeibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.
Zhong-Wei ZhouSchool of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.
Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEJena University Hospital · DESun Yat-sen University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNFriedrich Schiller University Jena · DEUniversity of Michigan–Ann Arbor · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MRE11, RAD50, and NBS1 form the MRN complex in response to DNA damage to activate ATM, a gene responsible for Ataxia-Telangiectasia (A-T). Loss of any components of the MRN complex compromises cell life. Mutations in

Indexed as

cerebellaMRE11NBS1neurodegenerationPurkinje neurons

Identifiers

PMID35153719
PMCPMC8831373
OpenAlexW4210466865

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.