Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of MCM8 deficiency on gene expression of mouse embryo fibroblasts

ABSTRACT: Effect of MCM8 deficiency on gene expression of mouse embryo fibroblasts

PROVIDER: PRJNA1068097 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27699728_1.fastq.gz	Fastqsanger.gz
	SRR27699728_2.fastq.gz	Fastqsanger.gz
	SRR27699729_1.fastq.gz	Fastqsanger.gz
	SRR27699729_2.fastq.gz	Fastqsanger.gz
	SRR27699730_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Effect of MCM8 deficiency on gene expression of mouse embryo fibroblasts

Project description:MCM8 is essential in the replication stress response to maintain genome stability during mitosis. The deficiency of MCM8 results in impaired proliferation and a prolonged cell cycle, which can decrease cell populations. To investigate the effect of MCM8 deficiency on gene expression, we conducted the RNA-seq in wildtype and Mcm8 knockout mouse embryo fibroblasts. We found that the majority of genes were co-expressed and the gene expression distribution was comparable between WT and KO MEFs, suggesting that the global transcription activity was not obviously affected after MCM8 deficiency. Analysis of differentially expressed genes (DEGs) showed they were enriched in pathways including stem cell differentiation and cell fate commitment. In addition, to determine whether MCM8 is potentially involved in regulating splicing, as strongly suggested by the MCM8 interactome, we also performed alternative splicing (AS) analysis on RNA-seq data. Our data suggested that MCM8 may not function in splicing.

2024-05-30 | GSE254004 | GEO

Effect of DKK1 on embryo elongation

Project description:Effect of DKK1 on embryo elongation

| PRJNA522975 | ENA

Effect of Ankrd31 deficiency in mouse testicular transcriptome

Project description:Effect of Ankrd31 deficiency in mouse testicular transcriptome

| PRJNA489193 | ENA

NLRP14 deficiency contributes to female infertility and early embryo arrest

Project description:Oocyte maturation is vital to attain full competence required fertilization and embryogenesis. As a maternal effect factor, NLRP14 is preferentially expressed in mammalian oocytes and early embryos. Yet the role and molecular mechanism of NLRP14 in oocyte maturation and early embryogenesis is largely unknown. Whether NLRP14 deficiency accounts for human infertility with oocyte and embryo defects remains to be elucidated. Here, NLRP14 is identified essential for establishment of competent oocytes that can sustain early embryo development. Maternal deficiency of Nlrp14 results in sterility characterized by oocyte maturation defects and early embryo arrest. Nlrp14 ablation leads to compromised oocyte quality and developmental competence due to impaired oocyte cytoplasmic and nuclear maturation. Mechanistically, NLRP14 interacts with UHRF1 in oocyte cytoplasm to protect it from proteasome-dependent degradation, and perturbs maternal mRNA zygotic-decay and zygotic genome activation during maternal-zygotic transition. Furthermore, compound heterozygous pathogenic variants in NLRP14 gene are identified in infertile women with early embryonic arrest, which interrupt the NLRP14-UHRF1 interaction or UHRF1 protein expression. Our data uncover a vital role of NLRP14 as a new cytoplasmic-specific modulator of UHRF1 in oocyte meiotic maturation and early embryogenesis, which should provide new insights into risk prediction and genetic diagnosis for female infertility.

2024-06-01 | GSE234001 | GEO

Proteomic mapping of fibroblasts from patients with HSP60 deficiency

Project description:Deficiency of the mitochondrial chaperone HSP60 has detrimental effects on the mitochondrial functions, and can in patient’s lead to hypomyelination disorder. The present study investigates the proteome in cultivated skin fibroblasts originating from two patients with HSP60 genetic variants and hypomyelination.

2025-09-11 | PXD048923 | Pride

Folliculin deficiency effect on Raw264.7 cells

Project description:Folliculin deficiency effect on Raw264.7 cells

| PRJNA473700 | ENA

Effect of mitochondria deficiency on senescence-associated gene expression

Project description:We used parkin âoverexpressing MRC5 fibroblasts to investigate the role of mitochondria deficiency on senescence-associated gene expression. RNA-seq analysis on proliferating and senescent Parkin-expressing MRC5 fibroblasts treated with CCCP (treated) or DMSO (Untreated).

2016-01-12 | E-GEOD-76125 | biostudies-arrayexpress

Developing mouse embryo

Project description:Developing mouse embryo

| PRJNA888039 | ENA

NLRP14 deficiency contributes to female infertility and early embryo arrest

Project description:NLRP14 deficiency contributes to female infertility and early embryo arrest

| PRJNA979177 | ENA

Erf chromatin binding-sites in E13.5 mouse embryo fibroblasts

Project description:We show that reduced dosage of ERF, which encodes an inhibitory ETS transcription factor directly bound by ERK1/2 , causes complex craniosynostosis (premature fusion of the cranial sutures) in humans and mice. Features of this newly recognized clinical disorder include multiple suture synostosis, craniofacial dysmorphism, Chiari malformation and language delay. Mice with functional Erf reduced to ~30% of normal exhibit postnatal multisuture synostosis; by contrast, embryonic calvarial development appears mildly delayed. Using chromatin immunoprecipitation in mouse embryonic fibroblasts and high-throughput sequencing, we find that ERF binds preferentially to distal regulatory elements containing RUNX or AP1 motifs. This work identifies ERF as a novel regulator of osteogenic stimulation by RAS-ERK signaling, potentially by competing with activating ETS factors in multifactor transcriptional complexes. Examination of Erf binding site in E13.5 mouse embryo fibroblasts, growing in the presence or absence of serum for 4 hours

2013-01-15 | E-GEOD-42936 | biostudies-arrayexpress

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