Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identifying differentially expressed genes (DEGs，including lncRNA and mRNA) between shNC and shNAT10 female germline stem cells (FGSCs)

ABSTRACT: Integrated analysis of long RNA-seq and RNA in situ conformation sequencing (RIC-seq) data was performed to identify genes and RNA-RNA interaction pairs altered upon Nat10 knockdown.

ORGANISM(S): Mus musculus

PROVIDER: GSE298163 | GEO | 2026/06/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	GSE298163_All.fpkm.anno.xls.gz	Xls
	GSE298163_shnat10VSshnc.All.fpkm.anno.xls.gz	Xls

Items per page:

1 - 3 of 3

Similar Datasets

Identifying differentially expressed genes (DEGs) between shNC and shGm26917 female germline stem cells (FGSCs) [RNA-Seq]

Project description:Integrated analysis of RNA-seq and Ribosome profiling and sequencing (Ribo-seq) data was performed to identify translation efficiency altered upon Gm26917 knockdown.

2026-06-18 | GSE304963 | GEO

Identifying differentially acetylated mRNA between female germline stem cells (FGSCs) and differentiated FGCs (Dif-FGCs)

Project description:By combining RNA-seq analysis of differentiation-induced transcriptional changes with genome-wide ac4C profiling (acRIP-seq), we systematically investigated how N4-acetylcytidine modification regulates gene expression programs driving cellular differentiation. Key differentiation regulators showing both ac4C modification and expression changes were prioritized for functional validation.

2026-06-18 | GSE298164 | GEO

MeRIP sequencing analysis of female germline stem cells (FGSCs)

Project description:YTHDF2 displays extensive-expression patterns during oocyte maturation and its deficiency causes female infertility in mice. However, its specific mechanism of regulation remains elusive due to the absence of suitable in vitro models. FGSCs possess the capacity for self-renewal and differentiation into oocytes to support reproduction. The successful establishment of a line of FGSCs provides a platform for scientific research on female fertility and oogenesis. To understand how YTHDF2 exerts its regulatory effects on FGSCs, we conducted MeRIP-seq assay in FGSCs and aimed to identified YTHDF2 target transcripts.

2025-07-26 | E-MTAB-14256 | biostudies-arrayexpress

RNA sequencing of small number germ cells including primordial germ cells (PGCs) collected from female embryonic 12.5 day (E12.5), Female germline stem cells (FGSCs), Germinal-stage oocytes (GV oocytes) and Meiosis II oocytes (MII oocytes)

Project description:Mammalian oogenesis is an intricate and coordinated process involving dramatic changes in the transcriptional architecture. Through the small number of cells RNA sequencing (RNA Seq), we comprehensively uncovered the transcriptome dynamics of the mouse PGCs, FGSCs, GV Oocytes and M II Oocytes using. These results would provide some valuable navigation for the mechanism research of mammalian FGSCs in the future.

2017-08-15 | GSE75738 | GEO

Next-Generation Sequencing of Usp7 Overexpression and Knockdown Female Germline Stem Cells (FGSCs) Transcriptomes

Project description:Next-generation sequencing (NGS) was performed to analyze the usp7 effects on FGSCs.

2023-07-17 | GSE155548 | GEO

MeRIP sequencing analysis of female germline stem cells (FGSCs)

Project description:MeRIP sequencing analysis of female germline stem cells (FGSCs)

| PRJEB77835 | ENA

Integrative Omics Reveals Subtle Molecular Perturbations Following Ischemic Conditioning in a Porcine Kidney Transplant Model

Project description:Background: Remote Ischemic Conditioning (RIC) has been proposed as a therapeutic intervention to circumvent the Ischemia/reperfusion injury (IRI) that is inherent to organ transplantation. Using a porcine kidney transplant model, we aimed to decipher the subclinical molecular effects of a RIC regime, compared to non-RIC controls. Methods: Kidney pairs (n = 8+8) were extracted from brain dead donor pigs and transplanted in juvenile recipient pigs following a period of cold ischemia. One of the two kidney recipients in each pair was subjected to RIC prior to kidney graft reperfusion, while the other served as non-RIC control. We designed a modern integrative Omics strategy combining transcriptomics, proteomics, and phosphoproteomics to deduce molecular signatures in kidney tissue that could be attributed to RIC. Results: In kidney grafts taken out 10 h after transplantation we detected minimal molecular perturbations following RIC compared to non-RIC at the transcriptome level, which was mirrored at the proteome level. In particular, we noted that RIC resulted in suppression of tissue inflammatory profiles. Furthermore, an accumulation of muscle extracellular matrix assembly proteins in kidney tissues was detected at the protein level, which may be in response to muscle tissue damage and/or fibrosis. Conclusions: Our data identifies subtle molecular phenotypes in porcine kidneys following RIC and this knowledge could potentially aid optimisation of remote ischaemia protocols in renal transplantation.

2021-09-04 | E-MTAB-10872 | biostudies-arrayexpress

NAT10 inhibition improves cellular phenotypes of Hutchinson-Gilford progeria syndrome by restoring the Transportin-1 pathway

Project description:In this experiment, we aim to examine the role of NAT10 inhibition in Hutchinson-Gilford progeria syndrome (HGPS), a rare but devastating premature ageing syndrome caused by a mutation in the LMNA gene. NAT10 inhibition improves HGPS cellular phenotypes by releasing Transportin-1 (TNPO1) from the cytoplasm, restoring the TNPO1 pathway and allowing hnRNPA1 and NUP153 nuclear import, TPR anchorage at the nuclear pore complexes and RanGTP gradient re-balancing. We have promoted NAT10 inhibition by two ways in normal or patient derived primary skin fibroblasts; the NAT10 inhibitor Remodelin, and an siRNA directly targeting NAT10 (siNAT10). In addition, we have also used an siRNA against TNPO1 and a combined siTNPO1 and siNAT10 treatment. This is a 2-factor design, with treatment (Remodelin vs untreated, or siNAT10 vs siCT) and condition (HGPS vs normal fibroblasts) as the two conditions. Transcriptional profiling was performed using HumanHT-12 v4 Expression BeadChip microarrays, and all conditions were run in triplicate.

2018-06-25 | E-MTAB-6651 | biostudies-arrayexpress

Translation efficiency (TE) changes between shNC and shGm26917 FGSCs were quantified by ribosome profiling (Ribo-seq) and RNA-seq integration [Ribo-Seq]

Project description:Integrated analysis of Ribo-seq and RNA-seq data was performed to identify translation efficiency altered upon Gm26917 knockdown, To assess changes in translational efficiency and validate Gm26917 function.

2026-06-18 | GSE304964 | GEO

NAT10-dependent N4-acetylcytidine (ac4C) reprograms R-loops and promotes cancer stem cell growth

Project description:R-loop remodeling dynamically regulates chromatin states and gene expression; however, its exploitation by cancer to sustain self-renewal and malignancy remains poorly understood. Here, we found that glioblastoma (GBM) stem cells (GSCs) display highly active R-loops compared to differentiated tumor progeny and neural stem cells (NSCs). Genome-wide mapping by R-loop RNA chromatin immunoprecipitation sequencing (RR-ChIP-seq) revealed cell-specific enrichment and spatial accumulation of R-loops at promoter-proximal regions in GSCs, correlating with active transcription and open chromatin states. We profiled R-loop interactomes and identified N-Acetyltransferase 10 (NAT10), an RNA N4-acetylcytidine (ac4C)-modifying enzyme, as a high-affinity R-loop-binding protein in GSCs. Driven by transcriptional activation via OLIG1, NAT10 was overexpressed in GSCs. ac4C-specific RNA immunoprecipitation sequencing (ac4C-RIP-seq) on R-loop RNA revealed genome-wide mapping of ac4C-modified R-loops with abundant ac4C-modified R-loops that regulated the genome. NAT10 catalyzed widespread ac4C deposition on the RNA stand of R-loops, stabilizing promoter-associated R-loops, and facilitating open chromatin to sustain self-renewal through core stemness regulators, including transcription factor EGR1. NAT10 knockdown suppressed proliferation and maintenance in vitro and attenuated tumor growth in vivo. Pharmacological inhibition of NAT10/ac4C-modified R-loops using the small-molecule inhibitor remodelin phenocopied NAT10 genetic targeting, demonstrating therapeutic promise for targeting cancer.

2026-04-10 | PXD077002 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data