Evidence map›Paper›PMID 27401717›Full record

ArticleNature communications2016

Claspin recruits Cdc7 kinase for initiation of DNA replication in human cells.

Chi-Chun Yang, Masahiro Suzuki, Shiori Yamakawa, Syuzi Uno, Ai Ishii, Satoshi Yamazaki, Rino Fukatsu, Ryo Fujisawa, Kenji Sakimura, Toshiki Tsurimoto and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

32 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Claspin and Cancer: Where Are We Now?International journal of molecular sciences · 2025
    Review
  5. ATR-CHK1 Axis Inhibitors in Gastric Cancer Treatment.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. The TIMELESS effort for timely DNA replication and protection.Cellular and molecular life sciences : CMLS · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Implications ofCancers · 2020
    Article
  20. 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 at 3 institutions in 1 country.

Chi-Chun YangDepartment of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, 4-6-1 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.
Masahiro SuzukiDepartment of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, 4-6-1 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.
Shiori YamakawaDepartment of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, 4-6-1 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.
Syuzi UnoDepartment of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, 4-6-1 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.
Ai IshiiDepartment of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, 4-6-1 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.
Satoshi YamazakiDepartment of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, 4-6-1 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.
Rino FukatsuDepartment of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, 4-6-1 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.
Ryo FujisawaDepartment of Biology, Faculty of Science, Kyushu University 744 Motooka, Nishi-ku, Fukuoka 819-0395, Japan.
Kenji SakimuraDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata 951-8585, Japan.
Toshiki TsurimotoDepartment of Biology, Faculty of Science, Kyushu University 744 Motooka, Nishi-ku, Fukuoka 819-0395, Japan.
Hisao MasaiDepartment of Genome Medicine, Tokyo Metropolitan Institute of Medical Science, 4-6-1 Kamikitazawa, Setagaya-ku, Tokyo 156-8506, Japan.
Tokyo Metropolitan Institute of Medical Science · JPKyushu University · JPNiigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Claspin transmits replication stress signal from ATR to Chk1 effector kinase as a mediator. It also plays a role in efficient replication fork progression during normal growth. Here we have generated conditional knockout of Claspin and show that Claspin knockout mice are dead by E12.5 and Claspin knockout mouse embryonic fibroblast (MEF) cells show defect in S phase. Using the mutant cell lines, we report the crucial roles of the acidic patch (AP) near the C terminus of Claspin in initiation of DNA replication. Cdc7 kinase binds to AP and this binding is required for phosphorylation of Mcm. AP is involved also in intramolecular interaction with a N-terminal segment, masking the DNA-binding domain and a newly identified PIP motif, and Cdc7-mediated phosphorylation reduces the intramolecular interaction. Our results suggest a new role of Claspin in initiation of DNA replication during normal S phase through the recruitment of Cdc7 that facilitates phosphorylation of Mcm proteins.

Indexed as

DNA ReplicationAdaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCell ProliferationCheckpoint Kinase 1DNA-Binding ProteinsGene Expression ProfilingGene Knockout TechniquesHEK293 CellsHeLa CellsHumansMiceMice, KnockoutPhosphorylationProtein Serine-Threonine KinasesAdaptor Proteins, Signal TransducingCDC7 protein, humanCdc7 protein, mouseCell Cycle ProteinsCheckpoint Kinase 1claspin protein, mouseDNA-Binding ProteinsProtein Serine-Threonine Kinases

Identifiers

PMID27401717
PMCPMC4945878
OpenAlexW2473145740

What OpenQuestion holds

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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.