Evidence map›Paper›PMID 24706997›Full record

ArticleJournal of radiation research2014

Hypersensitivity of mouse NEIL1-knockdown cells to hydrogen peroxide during S phase.

Ryohei Yamamoto, Yukari Ohshiro, Tatsuhiko Shimotani, Mizuki Yamamoto, Satoshi Matsuyama, Hiroshi Ide, Kihei Kubo

Open access · goldAbstract read
In one paragraph

Article in Journal of radiation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. 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

7 authors at 2 institutions in 1 country.

Ryohei YamamotoDepartment of Advanced Pathobiology, Graduate School of Life & Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai Kita, Izumisano, Osaka 598-8531, Japan yamamoto@vet.osakafu-u.ac.jp.
Yukari OhshiroDepartment of Advanced Pathobiology, Graduate School of Life & Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai Kita, Izumisano, Osaka 598-8531, Japan.
Tatsuhiko ShimotaniDepartment of Advanced Pathobiology, Graduate School of Life & Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai Kita, Izumisano, Osaka 598-8531, Japan.
Mizuki YamamotoDepartment of Advanced Pathobiology, Graduate School of Life & Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai Kita, Izumisano, Osaka 598-8531, Japan.
Satoshi MatsuyamaDepartment of Advanced Pathobiology, Graduate School of Life & Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai Kita, Izumisano, Osaka 598-8531, Japan.
Hiroshi IdeDepartment of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Kagamiyama, Higashi-Hiroshima, Hiroshima 739-8526, Japan.
Kihei KuboDepartment of Advanced Pathobiology, Graduate School of Life & Environmental Sciences, Osaka Prefecture University, 1-58 Rinku Ourai Kita, Izumisano, Osaka 598-8531, Japan.
Osaka Prefecture University · JPHiroshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative base damage occurs spontaneously due to reactive oxygen species generated as byproducts of respiration and other pathological processes in mammalian cells. Many oxidized bases are mutagenic and/or toxic, and most are repaired through the base excision repair pathway. Human endonuclease VIII-like protein 1 (hNEIL1) is thought to play an important role during the S phase of the cell cycle by removing oxidized bases in DNA replication fork-like (bubble) structures, and the protein level of hNEIL1 is increased in S phase. Compared with hNEIL1, there is relatively little information on the properties of the mouse ortholog mNEIL1. Since mouse cell nuclei lack endonuclease III-like protein (NTH) activity, in contrast to human cell nuclei, mNEIL1 is a major DNA glycosylase for repair of oxidized pyrimidines in mouse nuclei. In this study, we made mNEIL1-knockdown cells using an shRNA expression vector and examined the cell cycle-related variation in hydrogen peroxide (H2O2) sensitivity. Hypersensitivity to H2O2 caused by mNEIL1 knockdown was more significant in S phase than in G1 phase, suggesting that mNEIL1 has an important role during S phase, similarly to hNEIL1.

Indexed as

AnimalsCells, CulturedDNA DamageDNA GlycosylasesDNA RepairG1 PhaseGene Knockdown TechniquesHumansHydrogen PeroxideL CellsMiceRNA, Small InterferingS PhaseDNA GlycosylasesHydrogen PeroxideNEIL1 protein, humanNeil1 protein, mouseRNA, Small InterferingBERcell cycleglycosylasemouseNEIL1

Identifiers

PMID24706997
PMCPMC4100011
OpenAlexW2171787028

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.