Evidence map›Paper›PMID 37907898›Full record

ArticleBMC biology2023

PFTK1 kinase regulates axogenesis during development via RhoA activation.

Yasmilde Rodríguez González, Fatemeh Kamkar, Paymaan Jafar-Nejad, Suzi Wang, Dianbo Qu, Leticia Sanchez Alvarez, Dina Hawari, Margaret Sonnenfeld, Ruth S Slack, Paul R Albert and 2 more

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

Article in BMC biology, 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
0.3field-weighted citation impact, top 36% 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

12 authors at 2 institutions in 2 countries.

Yasmilde Rodríguez GonzálezDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Fatemeh KamkarDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Paymaan Jafar-NejadDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Suzi WangDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Dianbo QuDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Leticia Sanchez AlvarezDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Dina HawariDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Margaret SonnenfeldDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Ruth S SlackDepartment of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
Paul R AlbertOttawa Hospital Research Institute and Brain and Mind Research Institute, University of Ottawa, Ottawa, ON, K1H 8M5, Canada.
David S ParkDepartment of Clinical Neurosciences, Hotchkiss Brain Institute, University of Calgary, Calgary, AB, T2N 4N1, Canada. david.park1@ucalgary.ca.
Alvin JoselinDepartment of Clinical Neurosciences, Hotchkiss Brain Institute, University of Calgary, Calgary, AB, T2N 4N1, Canada. Alvin.Joselin1@ucalgary.ca.ORCID 0000-0002-9010-0421
University of Ottawa · CAUniversity of Calgary · CA

Funding

CIHR 148402CIHR FRN# 15123
6 · The paper itself

Abstract

backgroundPFTK1/Eip63E is a member of the cyclin-dependent kinases (CDKs) family and plays an important role in normal cell cycle progression. Eip63E expresses primarily in postnatal and adult nervous system in Drosophila melanogaster but its role in CNS development remains unknown. We sought to understand the function of Eip63E in the CNS by studying the fly ventral nerve cord during development.

resultsOur results demonstrate that Eip63E regulates axogenesis in neurons and its deficiency leads to neuronal defects. Functional interaction studies performed using the same system identify an interaction between Eip63E and the small GTPase Rho1. Furthermore, deficiency of Eip63E homolog in mice, PFTK1, in a newly generated PFTK1 knockout mice results in increased axonal outgrowth confirming that the developmental defects observed in the fly model are due to defects in axogenesis. Importantly, RhoA phosphorylation and activity are affected by PFTK1 in primary neuronal cultures. We report that GDP-bound inactive RhoA is a substrate of PFTK1 and PFTK1 phosphorylation is required for RhoA activity.

conclusionsIn conclusion, our work establishes an unreported neuronal role of PFTK1 in axon development mediated by phosphorylation and activation of GDP-bound RhoA. The results presented add to our understanding of the role of Cdks in the maintenance of RhoA-mediated axon growth and its impact on CNS development and axonal regeneration.

Indexed as

Cyclin-Dependent KinasesDrosophila melanogasterAnimalsCell CycleDrosophila ProteinsMiceNeuronsPhosphorylationProtein KinasesrhoA GTP-Binding Proteinrho GTP-Binding ProteinsCyclin-Dependent KinasesDrosophila ProteinsEip63E protein, DrosophilaPftk1 protein, mouseProtein KinasesRho1 protein, DrosophilarhoA GTP-Binding ProteinRhoA protein, mouserho GTP-Binding ProteinsAxogenesisCyclin-dependent kinasesEip63ENeuronal developmentPFTAIRERho

Identifiers

PMID37907898
PMCPMC10617079
OpenAlexW4388076868

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.