Evidence map›Paper›PMID 26256786›Full record

ArticleNeurobiology of aging2015

RNF8 deficiency results in neurodegeneration in mice.

Siwei Ouyang, Yanfeng Song, Yingxia Tian, Yibin Chen, Xiaochun Yu, Degui Wang

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of aging, 2015. 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
0.5field-weighted citation impact, top 34% 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, 46 citations in OpenAlex.

  1. Review
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  12. Spinal RNF20-Mediated Histone H2B Monoubiquitylation Regulates mGluR5 Transcription for Neuropathic Allodynia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
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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

6 authors at 2 institutions in 2 countries.

Siwei Ouyang *Department of Anatomy and Histology, Lanzhou University School of Basic Medical Sciences, Lanzhou, 730000, China.
Yanfeng Song *Department of Anatomy and Histology, Lanzhou University School of Basic Medical Sciences, Lanzhou, 730000, China.
Yingxia Tian *Department of Anatomy and Histology, Lanzhou University School of Basic Medical Sciences, Lanzhou, 730000, China.
Yibin ChenDepartment of Internal Medicine, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Xiaochun YuDepartment of Internal Medicine, The University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Degui WangDepartment of Anatomy and Histology, Lanzhou University School of Basic Medical Sciences, Lanzhou, 730000, China.
Lanzhou University · CNUniversity of Michigan–Ann Arbor · US

Funding

Regulation of Ionizing Radiation-Induced DNA Damage ResponseR01CA130899 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIU, YILUN · 2009 to 2023
$5.5M
Molecular Mechanisms of BRCA1-Dependent DNA Damage Response and TumorogenesisR01CA132755 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SHEN, BINGHUI · 2008 to 2019
$3.5M
Functional analysis of BRCA1 in DNA damage response and tumor suppressionR01CA187209 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI YU, XIAOCHUN · 2014 to 2018
$1.7M
Functional analysis of the TET2/OGT complex in epigenetic modificationsR01GM108647 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI YU, XIAOCHUN · 2015 to 2018
$1.3M
NCI NIH HHS R01 CA130899NCI NIH HHS R01 CA132755NCI NIH HHS R01 CA187209NIGMS NIH HHS R01 GM108647
6 · The paper itself

Abstract

The progressive loss of neurons causes neurodegenerative diseases. Because the accumulation of DNA breaks results in neuronal apoptosis, the lack of a variety of DNA damage repair-related proteins contributes to neurodegeneration. The ubiquitin ligase RNF8 plays an important role in DNA double-strand break repair via histone ubiquitination. However, the function of RNF8 in terminally differentiated neurons remains unknown. This study aimed to determine whether RNF8 is involved in the DNA damage response in neurons and contributes to neurodegeneration. Here, we present evidence suggesting that RNF8 deficiency results in DNA damage accumulation and neuronal apoptosis. RNF8(-/-) mice exhibit neuronal degeneration and reactive astrocytosis. Neurons from RNF8(-/-) mice appear to be more susceptible to X-ray-induced DNA damage. These changes were consistent with the behavioral performances of the RNF8-deficient mice, which included impaired performances in the open-field test and step-down avoidance task. Overall, these findings show that RNF8 is required for DNA damage repair in neurons. RNF8 deficiency is sufficient to cause neuronal pathology and cognitive decline, and the loss of RNF8 results in neuron degeneration.

Indexed as

AnimalsApoptosisCells, CulturedCognition DisordersDNADNA BreaksDNA DamageDNA RepairHistonesMiceNeurodegenerative DiseasesNeuronsUbiquitinationUbiquitin-Protein LigasesDNAHistonesRnf8 protein, mouseUbiquitin-Protein LigasesDNA damage repairDouble-strand breakNeurodegenerationRNF8Ubiquitin ligase

Identifiers

PMID26256786
PMCPMC4851709
OpenAlexW2161479083

What OpenQuestion holds

Textmetadata
LicenceTDM
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.