Evidence map›Paper›PMID 42059432›Full record

ArticleeLife2026

The FAM53C/DYRK1A axis regulates the G1/S transition of the cell cycle.

Taylar Hammond, Jong Bin Choi, Miles W Membreño, Janos Demeter, Roy Ng, Debadrita Bhattacharya, Thuyen N Nguyen, Griffin G Hartmann, Caterina I Colon, Carine Bossard and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Frontiers in cell and developmental biology · 2026
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Taylar HammondDepartments of Pediatrics, Stanford University, Stanford, United States.
Jong Bin ChoiDepartments of Pediatrics, Stanford University, Stanford, United States.ORCID https://orcid.org/0000-0002-7017-1775
Miles W MembreñoDepartment of Chemistry and Biochemistry, University of California, Santa Cruz, Santa Cruz, United States.
Janos DemeterDepartment of Microbiology and Immunology, Stanford University, Stanford, United States.
Roy NgDepartment of Microbiology and Immunology, Stanford University, Stanford, United States.ORCID https://orcid.org/0009-0004-4325-4753
Debadrita BhattacharyaDepartments of Pediatrics, Stanford University, Stanford, United States.ORCID https://orcid.org/0000-0002-1923-2675
Thuyen N NguyenDepartments of Pediatrics, Stanford University, Stanford, United States.
Griffin G HartmannDepartments of Pediatrics, Stanford University, Stanford, United States.
Caterina I ColonDepartments of Pediatrics, Stanford University, Stanford, United States.
Carine BossardBiosplice Therapeutics Inc, TenaRx Inc, San Diego, United States.ORCID https://orcid.org/0009-0005-2508-7282
Jan M SkotheimDepartment of Biology, Stanford University, Stanford, United States.ORCID https://orcid.org/0000-0001-8420-6820
Peter K JacksonDepartment of Microbiology and Immunology, Stanford University, Stanford, United States.ORCID https://orcid.org/0000-0002-1742-2539
Anca M PascaDepartments of Pediatrics, Stanford University, Stanford, United States.ORCID https://orcid.org/0000-0002-0445-9009
Seth M RubinDepartment of Chemistry and Biochemistry, University of California, Santa Cruz, Santa Cruz, United States.ORCID https://orcid.org/0000-0002-1670-4147
Julien SageDepartments of Pediatrics, Stanford University, Stanford, United States.ORCID https://orcid.org/0000-0002-8928-9968

Funding

Project 3: Defining and targeting mechanisms of E2F transcription factor regulationP01CA254867 · NCI · STANFORD UNIVERSITY · PI PETER Kent JACKSON · 2022 to 2026
$8.9M
NCI NIH HHS P01 CA254867NCI NIH HHS P01CA254867
6 · The paper itself

Abstract

A growing number of therapies are being developed to target the cell cycle machinery for the treatment of cancer and other human diseases. Consequently, a greater understanding of the factors regulating cell cycle progression becomes essential to help enhance the response to these new therapies. Here, using data from the Cancer Dependency Map, we identified FAM53C as a new regulator of cell cycle progression. We found that FAM53C is critical for this cell cycle transition and that it acts upstream of the Cyclin D-CDK4/6-RB axis and of p53 in the regulation of the G1/S transition. By mass spectrometry, biochemical, and cellular assays, we identified and validated DYRK1A as a cell cycle kinase that is inhibited by and directly interacts with FAM53C. Consistent with the role for FAM53C identified in cells in culture,

Indexed as

Cell Cycle ProteinsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesAnimalsCell CycleDyrk KinasesHumansMiceMice, KnockoutCell Cycle ProteinsDyrk KinasesProtein Serine-Threonine KinasesProtein-Tyrosine Kinasescell biologycell cycleCyclin DDYRK1AmouseRB

Identifiers

PMID42059432
PMCPMC13132546

What OpenQuestion holds

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LicenceCC BY
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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.