Evidence map›Paper›PMID 25737283›Full record

ArticleGenes & development2015

Cyclin-dependent kinase regulates the length of S phase through TICRR/TRESLIN phosphorylation.

Courtney G Sansam, Duane Goins, Joseph C Siefert, Emily A Clowdus, Christopher L Sansam

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing 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

45 citing papers in PubMed, 58 citations in OpenAlex.

  1. CDC7 and APC/CNature communications · 2026
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  8. Cell cycle control of cohesion establishment.bioRxiv : the preprint server for biology · 2025
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  18. LSD1 is required for euchromatic origin firing and replication timing.Signal transduction and targeted therapy · 2022
    Article
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  20. 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

5 authors at 2 institutions in 1 country.

Courtney G SansamCell Cycle and Cancer Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA; chris-sansam@omrf.org.
Duane GoinsCell Cycle and Cancer Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA;
Joseph C SiefertCell Cycle and Cancer Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA; Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.
Emily A ClowdusCell Cycle and Cancer Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA; Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.
Christopher L SansamCell Cycle and Cancer Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma 73104, USA; Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA chris-sansam@omrf.org.
University of Oklahoma Health Sciences Center · USOklahoma Medical Research Foundation · US

Funding

Proteomics CoreP20GM103447 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI DARRIN R. AKINS · 2012 to 2026
$60.2M
Understanding connective tissue development and disease with PDGFR-driven..... P20GM103636 · NIGMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI THOMPSON, LINDA F · 2013 to 2023
$26.9M
NIGMS NIH HHS 5P20GM103636-02NIGMS NIH HHS 8P20GM103447NIGMS NIH HHS P20 GM103447NIGMS NIH HHS P20 GM103636
6 · The paper itself

Abstract

S-phase cyclin-dependent kinases (CDKs) stimulate replication initiation and accelerate progression through the replication timing program, but it is unknown which CDK substrates are responsible for these effects. CDK phosphorylation of the replication factor TICRR (TopBP1-interacting checkpoint and replication regulator)/TRESLIN is required for DNA replication. We show here that phosphorylated TICRR is limiting for S-phase progression. Overexpression of a TICRR mutant with phosphomimetic mutations at two key CDK-phosphorylated residues (TICRR(TESE)) stimulates DNA synthesis and shortens S phase by increasing replication initiation. This effect requires the TICRR region that is necessary for its interaction with MDM two-binding protein. Expression of TICRR(TESE) does not grossly alter the spatial organization of replication forks in the nucleus but does increase replication clusters and the number of replication forks within each cluster. In contrast to CDK hyperactivation, the acceleration of S-phase progression by TICRR(TESE) does not induce DNA damage. These results show that CDK can stimulate initiation and compress the replication timing program by phosphorylating a single protein, suggesting a simple mechanism by which S-phase length is controlled.

Indexed as

Cell Cycle ProteinsCell Line, TumorCyclin-Dependent KinasesDNA DamageDNA ReplicationGene Expression RegulationHumansMutationPhosphorylationSignal TransductionS PhaseCell Cycle ProteinsCyclin-Dependent KinasesTICRR protein, humancell cyclecyclin-dependent kinaseDNA replicationreplication initiationreplication timingS phaseTICRR

Identifiers

PMID25737283
PMCPMC4358407
OpenAlexW2022784838

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.