Evidence map›Paper›PMID 33395410›Full record

ArticlePLoS biology2021

Cyclin-dependent Kinase 1 and Aurora Kinase choreograph mitotic storage and redistribution of a growth factor receptor.

Christina D Cota, Matthew S Dreier, William Colgan, Anna Cha, Twan Sia, Brad Davidson

Open access · goldAbstract read
In one paragraph

Article in PLoS biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Cell numbers contribute to cell fate during Ciona cardiopharyngeal mesoderm specification.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. CDK1-loaded extracellular vesicles promote cell cycle to reverse impaired wound healing in diabetic obese mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  3. Article
  4. Investigating cellular dynamics in tunicates.Genesis (New York, N.Y. : 2000) · 2023
    Article
  5. Article
  6. 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

6 authors at 5 institutions in 1 country.

Christina D CotaDepartment of Biology, Colby College, Waterville, Maine, United States of America.ORCID 0000-0003-1307-903X
Matthew S DreierNYU Grossman School of Medicine, New York, New York, United States of America.
William ColganBroad Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America.ORCID 0000-0002-8328-4672
Anna ChaDepartment of Molecular & Cellular Biology, Harvard University, Cambridge, Massachusetts, United States of America.
Twan SiaDepartment of Biology, Swarthmore College, Swarthmore, Pennsylvania, United States of America.
Brad DavidsonDepartment of Biology, Swarthmore College, Swarthmore, Pennsylvania, United States of America.
Swarthmore College · USBroad Institute · USColby College · USHarvard University · USNew York University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endosomal trafficking of receptors and associated proteins plays a critical role in signal processing. Until recently, it was thought that trafficking was shut down during cell division. Thus, remarkably, the regulation of trafficking during division remains poorly characterized. Here we delineate the role of mitotic kinases in receptor trafficking during asymmetric division. Targeted perturbations reveal that Cyclin-dependent Kinase 1 (CDK1) and Aurora Kinase promote storage of Fibroblast Growth Factor Receptors (FGFRs) by suppressing endosomal degradation and recycling pathways. As cells progress through metaphase, loss of CDK1 activity permits differential degradation and targeted recycling of stored receptors, leading to asymmetric induction. Mitotic receptor storage, as delineated in this study, may facilitate rapid reestablishment of signaling competence in nascent daughter cells. However, mutations that limit or enhance the release of stored signaling components could alter daughter cell fate or behavior thereby promoting oncogenesis.

Indexed as

AnimalsAnimals, Genetically ModifiedAurora KinasesCDC2 Protein KinaseCell Cycle ProteinsCiona intestinalisEmbryo, NonmammalianMitosisProtein TransportReceptors, Fibroblast Growth FactorReceptors, Growth FactorSignal TransductionTissue DistributionAurora KinasesCDC2 Protein KinaseCell Cycle ProteinsReceptors, Fibroblast Growth FactorReceptors, Growth Factor

Identifiers

PMID33395410
PMCPMC7808676
OpenAlexW3118372230

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.