Evidence map›Paper›PMID 34680909›Full record

ArticleGenes2021

Isorhamnetin Promotes 53BP1 Recruitment through the Enhancement of ATM Phosphorylation and Protects Mice from Radiation Gastrointestinal Syndrome.

Yuichi Nishiyama, Akinori Morita, Shogo Tatsuta, Misaki Kanamaru, Masahiro Sakaue, Kenta Ueda, Manami Shono, Rie Fujita, Bing Wang, Yoshio Hosoi and 2 more

Open access · goldAbstract read
In one paragraph

Article in Genes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 30% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. 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

12 authors at 5 institutions in 1 country.

Yuichi NishiyamaGraduate School of Biomedical Sciences, Tokushima University, Tokushima 770-8503, Japan.ORCID 0000-0001-8960-6110
Akinori MoritaGraduate School of Biomedical Sciences, Tokushima University, Tokushima 770-8503, Japan.ORCID 0000-0001-9988-6136
Shogo TatsutaGraduate School of Biomedical Sciences, Tokushima University, Tokushima 770-8503, Japan.
Misaki KanamaruGraduate School of Biomedical Sciences, Tokushima University, Tokushima 770-8503, Japan.
Masahiro SakaueGraduate School of Biomedical Sciences, Tokushima University, Tokushima 770-8503, Japan.
Kenta UedaGraduate School of Biomedical Sciences, Tokushima University, Tokushima 770-8503, Japan.
Manami ShonoGraduate School of Biomedical Sciences, Tokushima University, Tokushima 770-8503, Japan.
Rie FujitaFaculty of Pharmacy, Keio University, Tokyo 105-8512, Japan.
Bing WangNational Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, Chiba 263-8555, Japan.ORCID 0000-0002-7180-639X
Yoshio HosoiDepartment of Radiation Biology, Graduate School of Medicine, Tohoku University, Sendai 980-8575, Japan.
Shin AokiFaculty of Pharmaceutical Sciences, Tokyo University of Science, Chiba 278-8510, Japan.ORCID 0000-0002-4287-6487
Takeshi SugaiFaculty of Pharmacy, Keio University, Tokyo 105-8512, Japan.
Tokushima University · JPKeio University · JPNational Institutes for Quantum Science and Technology · JPTohoku University · JPTokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Flavonoids are a subclass of polyphenols which are attractive, due to possessing various physiological activities, including a radioprotective effect. Tumor suppressor p53 is a primary regulator in the radiation response and is involved in the pathogenesis of radiation injuries. In this study, we revealed that isorhamnetin inhibited radiation cell death, and investigated its action mechanism focusing on DNA damage response. Although isorhamnetin moderated p53 activity, it promoted phosphorylation of ataxia telangiectasia mutated (ATM) and enhanced 53BP1 recruitment in irradiated cells. The radioprotective effect of isorhamnetin was not observed in the presence of ATM inhibitor, indicating that its protective effect was dependent on ATM. Furthermore, isorhamnetin-treated mice survived gastrointestinal death caused by a lethal dose of abdominal irradiation. These findings suggested that isorhamnetin enhances the ATM-dependent DNA repair process, which is presumably associated with the suppressive effect against GI syndrome.

Indexed as

Acute Radiation SyndromeAnimalsAtaxia Telangiectasia Mutated ProteinsFemaleHep G2 CellsHumansIntestinal MucosaMiceMice, Inbred ICRPhosphorylationQuercetinRadiation-Protective AgentsTumor Suppressor p53-Binding Protein 13-methylquercetinAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseQuercetinRadiation-Protective AgentsTrp53bp1 protein, mouseTumor Suppressor p53-Binding Protein 153BP1ATMDNA damage responseisorhamnetinp53p53 target genespS1981-ATMradiation gastrointestinal syndromeradiation hematopoietic syndromeγH2AX

Identifiers

PMID34680909
PMCPMC8535534
OpenAlexW3204663186

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.