Evidence map›Paper›PMID 31272276›Full record

ArticleCell cycle (Georgetown, Tex.)2019

Clathrin heavy chain phosphorylated at T606 plays a role in proper cell division.

Yusuke Yabuno, Toshihiro Uchihashi, Towa Sasakura, Hiroyuki Shimizu, Yoko Naito, Kohshiro Fukushima, Kaori Ota, Mikihiko Kogo, Hiroshi Nojima, Norikazu Yabuta

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2019. 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
0.9field-weighted citation impact, top 18% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. 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

10 authors at 2 institutions in 1 country.

Yusuke Yabunoa First Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University , Osaka , Japan.
Toshihiro Uchihashia First Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University , Osaka , Japan.
Towa Sasakurab Department of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University , Osaka , Japan.
Hiroyuki Shimizub Department of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University , Osaka , Japan.
Yoko Naitob Department of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University , Osaka , Japan.ORCID 0000-0003-1512-3313
Kohshiro Fukushimab Department of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University , Osaka , Japan.
Kaori Otab Department of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University , Osaka , Japan.
Mikihiko Kogoa First Department of Oral and Maxillofacial Surgery, Graduate School of Dentistry, Osaka University , Osaka , Japan.
Hiroshi Nojimab Department of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University , Osaka , Japan.
Norikazu Yabutab Department of Molecular Genetics, Research Institute for Microbial Diseases, Osaka University , Osaka , Japan.
The University of Osaka · JPAichi Cancer Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clathrin regulates mitotic progression, in addition to membrane trafficking. However, the detailed regulatory mechanisms of clathrin during mitosis remain elusive. Here, we demonstrate novel regulation of clathrin during mitotic phase of the cell cycle. Clathrin heavy chain (CHC) was phosphorylated at T606 by its association partner cyclin G-associated kinase (GAK). This phosphorylation was required for proper cell proliferation and tumor growth of cells implanted into nude mice. Immunofluorescence analysis showed that the localization of CHC-pT606 signals changed during mitosis. CHC-pT606 signals localized in the nucleus and at the centrosome during interphase, whereas CHC signals were mostly cytoplasmic. Co-immunoprecipitation suggested that CHC formed a complex with GAK and polo-like kinase 1 (PLK1). Depletion of GAK using siRNA induced metaphase arrest and aberrant localization of CHC-pT606, which abolished Kiz-pT379 (as a phosphorylation target of PLK1) signals on chromatin at metaphase. Taken together, we propose that the GAK_CHC-pT606_PLK1_Kiz-pT379 axis plays a role in proliferation of cancer cells.

Indexed as

AnimalsCell Cycle ProteinsCell NucleusCentrosomeClathrin Heavy ChainsFemaleGene Knockdown TechniquesHeLa CellsHeterograftsHumansInterphaseIntracellular Signaling Peptides and ProteinsMetaphaseMiceMice, Inbred BALB CMice, NudeCell Cycle ProteinsClathrin Heavy ChainsCLTC protein, humanGAK protein, humanIntracellular Signaling Peptides and ProteinsPolo-Like Kinase 1Protein Serine-Threonine KinasesProto-Oncogene ProteinscentrosomeCHCGAKKizunamitosisPLK1

Identifiers

PMID31272276
PMCPMC6681784
OpenAlexW2955698893

What OpenQuestion holds

Textmetadata
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.