Evidence map›Paper›PMID 39687386›Full record

ArticleData in brief2024

Proteomic dataset of knockdown of AKT3 on protein expression and function in female germline stem cells.

Yue Shen, Chunlan Mu, Qingling Jia, Xiaoyong Li, Ji Wu

Abstract read
In one paragraph

Article in Data in brief, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Yue ShenKey Laboratory of Fertility Preservation and Maintenance of Ministry of Education, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.
Chunlan MuKey Laboratory of Fertility Preservation and Maintenance of Ministry of Education, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.
Qingling JiaKey Laboratory of Fertility Preservation and Maintenance of Ministry of Education, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.
Xiaoyong LiKey Laboratory for the Genetics of Developmental & Neuropsychiatric Disorders (Ministry of Education), Bio-X Institutes, Shanghai Jiao Tong University, Shanghai 200240, China.
Ji WuKey Laboratory of Fertility Preservation and Maintenance of Ministry of Education, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Female germline stem cells (FGSCs) are adult stem cells capable of self-renewal and differentiation into mature oocytes. AKT3, a member of the AKT kinase family, plays crucial roles in multiple cellular processes, such as proliferation, migration, and apoptosis. However, the mechanism by which AKT3 affects the development of FGSCs is poorly understood. We performed 4D-data-independent acquisition (DIA) Quantitative Proteomics on mouse FGSCs in which AKT3 was knocked down using a lentivirus and on control FGSCs. Based on the raw DIA data, coupled with database searches and data filtering, we identified 46,260 peptides, including 45,821 unique peptides, corresponding to 6849 identified proteins and 6697 comparable proteins. These identified proteins were functionally annotated using Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), Protein Domain, Clusters of Orthologous Genes (COG)/Eukaryotic Orthologous Groups (KOG), STRING database, Reactome, WikiPathways, HallMark, and transcription factor (TF) analyses. Fisher's exact test was used to assess the significance of functional enrichment of the differentially abundant proteins. We identified 281 differentially abundant proteins between AKT3 knockdown and control FGSCs, comprising 229 upregulated and 52 downregulated proteins. We performed clustering analysis on these differentially abundant proteins based on functional enrichment using GO, Domain, KEGG, Reactome and WikiPathways platforms. A protein-protein interaction network was constructed to demonstrate interactions between proteins. These datasets will facilitate future investigations into the mechanisms governing FGSC self-renewal and differentiation and will provide a foundation for understanding diseases related to abnormal germ cell development.

Indexed as

FGSCsPathway analysisProteomics

Identifiers

PMID39687386
PMCPMC11647134

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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.