Evidence map›Paper›PMID 39097652›Full record

ArticleScientific reports2024

PTIP epigenetically regulates DNA damage-induced cell cycle arrest by upregulating PRDM1.

Yuichiro Nakata, Shion Nagasawa, Yasuyuki Sera, Norimasa Yamasaki, Akinori Kanai, Kohei Kobatake, Takeshi Ueda, Miho Koizumi, Ichiro Manabe, Osamu Kaminuma and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. PAX-Interacting Protein 1 (PTIP) Promotes Apoptosis.Journal of cellular signaling · 2025
    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

11 authors.

Yuichiro Nakata *Department of Systems Medicine, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8670, Japan. nakatay@chiba-u.jp.
Shion Nagasawa *Department of Systems Medicine, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8670, Japan.
Yasuyuki SeraField of Human Disease Models, Major in Advanced Life Sciences and Medicine,, Institute of Laboratory Animals, Tokyo Women's Medical University, 8-1 Kawada-Cho, Shinjuku-Ku, Tokyo, 162-8666, Japan.
Norimasa YamasakiDepartment of Disease Models, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-Ku, Hiroshima, 734-8553, Japan.
Akinori KanaiLaboratory of Systems Genomics, Department of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, 5-1-5 Kashiwanoha, Kashiwa, Chiba, 277-8561, Japan.
Kohei KobatakeDepartment of Urology, Institute of Biomedical and Health Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-Ku, Hiroshima, 734-8553, Japan.
Takeshi UedaDepartment of Biochemistry, Faculty of Medicine, Kindai University, 377-2 Ohnohigashi, Osakasayama-Shi, Osaka, 589-8511, Japan.
Miho KoizumiField of Human Disease Models, Major in Advanced Life Sciences and Medicine,, Institute of Laboratory Animals, Tokyo Women's Medical University, 8-1 Kawada-Cho, Shinjuku-Ku, Tokyo, 162-8666, Japan.
Ichiro ManabeDepartment of Systems Medicine, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-Ku, Chiba-Shi, Chiba, 260-8670, Japan.
Osamu KaminumaDepartment of Disease Models, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-Ku, Hiroshima, 734-8553, Japan.
Hiroaki HondaField of Human Disease Models, Major in Advanced Life Sciences and Medicine,, Institute of Laboratory Animals, Tokyo Women's Medical University, 8-1 Kawada-Cho, Shinjuku-Ku, Tokyo, 162-8666, Japan. honda.hiroaki@twmu.ac.jp.

Funding

AMED-CREST JP24gm1310006JSPS KAKENHI 18K16087
6 · The paper itself

Abstract

The genome is constantly exposed to DNA damage from endogenous and exogenous sources. Fine modulation of DNA repair, chromatin remodeling, and transcription factors is necessary for protecting genome integrity, but the precise mechanisms are still largely unclear. We found that after ionizing radiation (IR), global trimethylation of histone H3 at lysine 4 (H3K4me3) was decreased at an early (5 min) post-IR phase but increased at an intermediate (180 min) post-IR phase in both human and mouse hematopoietic cells. We demonstrated that PTIP, a component of the MLL histone methyltransferase complex, is required for H3K4me3 upregulation in the intermediate post-IR phase and promotes cell cycle arrest by epigenetically inducing a cell cycle inhibitor, PRDM1. In addition, we found that PTIP expression is specifically downregulated in acute myeloid leukemia patients. These findings collectively suggest that the PTIP-PRDM1 axis plays an essential role in proper DNA damage response and its deregulation contributes to leukemogenesis.

Indexed as

Cell Cycle CheckpointsDNA-Binding ProteinsDNA DamagePositive Regulatory Domain I-Binding Factor 1AnimalsCarrier ProteinsEpigenesis, GeneticHistonesHumansLeukemia, Myeloid, AcuteMiceNuclear ProteinsRadiation, IonizingUp-RegulationCarrier ProteinsDNA-Binding Proteinshistone H3 trimethyl Lys4HistonesNuclear ProteinsPAXIP1 protein, humanPaxip1 protein, mousePositive Regulatory Domain I-Binding Factor 1PRDM1 protein, humanDNA damage responseH3K4me3Histone methylationPTIP

Identifiers

PMID39097652
PMCPMC11297997

What Socratic 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 Socratic graph.