Evidence map›Paper›PMID 36759599›Full record

ArticleCell death & disease2023

The phosphorylation of PHF5A by TrkA-ERK1/2-ABL1 cascade regulates centrosome separation.

Chen Song, Yu Zhang, Yutong Li, Juntao Bie, Zhe Wang, Xin Yang, Haishuang Li, Liangyi Zhu, Tianzhuo Zhang, Qing Chang and 1 more

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

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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 1 institution in 2 countries.

Chen SongDepartment of Medical Genetics, Center for Medical Genetics, Peking University Health Science Center, Beijing, 100191, China.
Yu ZhangDepartment of Medical Genetics, Center for Medical Genetics, Peking University Health Science Center, Beijing, 100191, China.
Yutong LiDepartment of Medical Genetics, Center for Medical Genetics, Peking University Health Science Center, Beijing, 100191, China.
Juntao BieDepartment of Medical Genetics, Center for Medical Genetics, Peking University Health Science Center, Beijing, 100191, China.
Zhe WangDepartment of Medical Genetics, Center for Medical Genetics, Peking University Health Science Center, Beijing, 100191, China.
Xin YangDepartment of Medical Genetics, Center for Medical Genetics, Peking University Health Science Center, Beijing, 100191, China.
Haishuang LiDepartment of Pathology, Peking University School of Basic Medical Science; Peking University Third Hospital, Peking University Health Science Center, Beijing, 100191, China.
Liangyi ZhuDepartment of Pathology, Peking University School of Basic Medical Science; Peking University Third Hospital, Peking University Health Science Center, Beijing, 100191, China.
Tianzhuo ZhangDepartment of Medical Genetics, Center for Medical Genetics, Peking University Health Science Center, Beijing, 100191, China.
Qing ChangDepartment of Pathology, Peking University School of Basic Medical Science; Peking University Third Hospital, Peking University Health Science Center, Beijing, 100191, China. qingchang@bjmu.edu.cn.
Jianyuan LuoDepartment of Medical Genetics, Center for Medical Genetics, Peking University Health Science Center, Beijing, 100191, China. luojianyuan@bjmu.edu.cn.ORCID 0000-0001-6057-2914
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During interphase, the newly duplicated pairs of centrosomes are held together by a centrosome linker, and the centrosome separation needs the disruption of this linker to induce the duplicated centrosomes separating into two distinct microtubule organization centers. The mechanism of regulating centrosome separation is however poorly understood. Here, we demonstrated that the phosphorylation of PHF5A at Y36 by the TrkA-ERK1/2-ABL1 cascade plays a critical role in regulating centrosome separation. PHF5A, a well-characterized spliceosome component, is enriched in the centrosome. The pY36-PHF5A promotes the interaction between CEP250 and Nek2A in a spliceosomal-independent manner, which leads to premature centrosome separation. Furthermore, the unmatured centrosome remodels the microtubule and subsequently regulates cell proliferation and migration. Importantly, we found that the phosphorylation cascade of TrkA-ERK1/2-ABL1-PHF5A is hyper-regulated in medulloblastoma. The inhibition of this cascade can induce senescence and restrict the proliferation of medulloblastoma. Our findings on this phosphorylation cascade in regulating centrosome separation could provide a series of potential targets for restricting the progress of medulloblastoma.

Indexed as

Cerebellar NeoplasmsMedulloblastomaAutoantigensCell Cycle ProteinsCentrosomeHeLa CellsHumansMAP Kinase Signaling SystemMicrotubulesNIMA-Related KinasesPhosphorylationProtein Serine-Threonine KinasesReceptor Protein-Tyrosine KinasesRNA-Binding ProteinsTrans-ActivatorsAutoantigensCell Cycle ProteinsCEP250 protein, humanNIMA-Related KinasesPHF5A protein, humanProtein Serine-Threonine KinasesReceptor Protein-Tyrosine KinasesRNA-Binding ProteinsTrans-Activators

Identifiers

PMID36759599
PMCPMC9911754
OpenAlexW4319812551

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.