Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome-wide analysis upon DCP1A knockout

ABSTRACT: We analyzed the effect of DCP1A knockout on total RNA population in undifferentiated mouse embryonic stem cells

ORGANISM(S): Mus musculus

PROVIDER: GSE118919 | GEO | 2020/06/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Genome-wide mapping of active RNA polymerases using precision nuclear run-on (PRO-seq) upon DCP1A knockout

Project description:We analyzed the effect of DCP1A knockout on nascent transcripts population in undifferentiated mouse embryonic stem cells

2020-06-25 | GSE118930 | GEO

Transcriptome-wide analysis upon DCP1A knockout

Project description:Transcriptome-wide analysis upon DCP1A knockout

| PRJNA487346 | ENA

DCP1A knockout: transcriptome-wide characterization

Project description:DCP1A knockout: transcriptome-wide characterization

| PRJNA487454 | ENA

Cordycepin Delays Postovulatory Aging of Mammalian Oocytes through Inhibition of Maternal mRNAs Degradation via DCP1A Polyadenylation Suppression

Project description:Postovulatory aging leads to the decline in oocyte quality and subsequent impairment of embryonic development, thereby reducing the success rates of assisted reproductive technology (ART). Nevertheless, potential preventative strategies to improve aging oocytes quality and the associated underlying mechanisms warrant further investigation. In this study, we identify cordycepin, an natural nucleoside analogue, as having the potential to restore the postovulatory aging-induced decline in oocyte quality, including aspects such as oocyte fragmentation, embryonic developmental competence, spindle/chromosomes morphology and mitochondrial function. Proteomic and RNA sequencing analyses revealed that cordycepin inhibited the degradation of several crucial maternal proteins and mRNAs caused by aging. Mechanistically, cordycepin was found to suppress the elevation of DCP1A protein levels by inhibiting polyadenylation during postovulatory aging, consequently impeding the decapping of maternal mRNAs. In humans, the increased degradation of DCP1A and total mRNA during aging was also inhibited by cordycepin. Collectively, our findings demonstrate that cordycepin may prevent postovulatory aging of mammalian oocytes by inhibition of maternal mRNAs degradation via DCP1A polyadenylation suppression, thereby promoting the successful rates of ART procedure.

2024-01-26 | PXD042600 | Pride

Effects of Dcp1a and Dcp2 knockdown during mouse oocyte maturation

Project description:Oocyte maturation is accompanied by a transition from mRNA stability to instability. We investigated the role of DCP1A and DCP2, proteins responsible for mRNA decapping, in mRNA destabilization during mouse oocyte maturation. siRNA-mediated knockdown of both Dcp1a and Dcp2 transcripts prior to initiation of maturation inhibited the maturation-associated increase of DCP1A and DCP2, stabilized a set of maternal mRNAs that are normally degraded during maturation, and inhibited development beyond the 2-cell stage, likely a consequence of failure to activate fully the zygotic genome. Total RNA from 30 MII eggs was used in each sample. Three independent biological replicates were analyzed for each condition.

2013-02-06 | E-GEOD-27049 | biostudies-arrayexpress

Genome-wide mapping of active RNA polymerases using precision nuclear run-on (PRO-seq) upon DCP1A knockout

Project description:Genome-wide mapping of active RNA polymerases using precision nuclear run-on (PRO-seq) upon DCP1A knockout

| PRJNA487350 | ENA

Dcp1a, a novel Mek substrate, regulates the self-renewal and differentiation of mouse embryonic stem cells

Project description:Mek inhibitor is widely applied to maintain pluripotency, while prolonged Mek inhibition compromises the developmental potential of mouse embryonic stem cells (ESCs). To better understand the mechanism of Mek in pluripotency maintenance, we first demonstrated that Mek regulates gene expression at post-transcriptional steps. Consistently, many of the 66 Mek substrates identified by quantitative phosphoproteomic analysis are involved in RNA processing. We further confirmed that S563 of Dcp1a, a mRNA decapping cofactor and P-body component, is phosphorylated by Mek1. Dcp1a, as well as two other P-body components Edc4 and Dcp2, are required for the proper self-renewal and differentiation of ESCs, indicating the role of P-bodies in ESCs. Dephosphorylation of Dcp1a S563 facilitates both self-renewal and differentiation of ESCs, through promoting P-body formation and RNA storage. In summary, our study identified 66 Mek substrates supporting the Erk-independent function of Mek, and revealed that Dcp1a, phosphorylated by Mek, regulates ESC self-renewal and differentiation, through modulating P-body formation.

2024-11-19 | GSE269161 | GEO

Effects of Dcp1a and Dcp2 knockdown during mouse oocyte maturation

2013-02-06 | GSE27049 | GEO

Dcp1a, a novel Mek substrate, regulates the self-renewal and differentiation of mouse embryonic stem cells [Ribo-seq]

2024-11-19 | GSE267674 | GEO

Dcp1a, a novel Mek substrate, regulates the self-renewal and differentiation of mouse embryonic stem cells [RNA-seq]

2024-11-19 | GSE267668 | GEO