Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

E-MEXP-2218

ABSTRACT: Transcription profiling of human MCF7 cell line with siRNA mediated knockdown of CNOT7 and/or CNOT8 subunits of Ccr4-Not deadenylase compared to control

PROVIDER: E-MEXP-2218 | ExpressionAtlas | 2025-01-22

REPOSITORIES: ExpressionAtlas

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	E-MEXP-2218-analysis-methods.tsv	Tabular
	E-MEXP-2218-atlasExperimentSummary.Rdata	Rdata
	E-MEXP-2218-configuration.xml	Xml
	E-MEXP-2218-percentile-ranks.tsv	Tabular
	E-MEXP-2218.condensed-sdrf.tsv	Tabular

Items per page:

1 - 5 of 83

Similar Datasets

The CCR4-NOT complex suppresses untimely translational activation of maternal mRNAs.

Project description:Control of mRNA poly(A) tail has central role to regulate mRNA metabolism: translation efficiency and mRNA stability. Gene expression in maturing oocytes largely relies on the regulation of mRNA metabolism as they are transcriptionally silent. The CCR4-NOT complex is a major deadenylase for mammals and regulates poly(A) tails of maternal mRNAs, however their function to translational regulation was not well understood. Here we show that CCR4-NOT suppresses translational activity of maternal mRNAs during oocyte maturation. Oocytes which lack entire deadenylase activity of CCR4-NOT by genetic deletion of its catalytic subunits: CNOT7 and CNOT8 showed increase of both expression of maternal mRNAs and translational activity of them during oocyte maturation.

2023-10-01 | GSE224308 | GEO

Transcription profiling of human MCF7 cell line with siRNA mediated knockdown of CNOT7 and/or CNOT8 subunits of Ccr4-Not deadenylase compared to control

Project description:siRNA-mediated knockdown of CNOT7 and/or CNOT8 compared to control to study role in the regulation of gene expression by these factors.

2009-07-15 | E-MEXP-2218 | biostudies-arrayexpress

RNAi profiling by array of human MCF7 cells with siRNA-mediated knockdown of CNOT6 and/or CNOT6L, or CNOT7 and CNOT8

Project description:siRNA-mediated knockdown of CNOT6 and/or CNOT6L, or CNOT7 and CNOT8 compared to control to study role in the regulation of gene expression by these factors.

2011-09-14 | E-MEXP-2926 | biostudies-arrayexpress

The CNOT4 Subunit of the CCR4-NOT Complex is Involved in mRNA Degradation, Efficient DNA Damage Repair, and XY Chromosome Crossover during Male Germ Cell Meiosis

Project description:The CCR4-NOT complex is a major mRNA deadenylase in eukaryotes and comprise CNOT6/6L and CNOT7/8, both of which are two types of catalytic subunits, as well as CNOT4, which is a regulatory subunit with previously undetermined functions. These subunits are previously hypothesized to play synergistic biochemical functions; however, their in vivo functions have remained poorly investigated. In this study, we constructed viable Cnot6/6l double knockout mice and the males were fertile, whereas Cnot7–/– male mice have been reported to be infertile. These results are against canonical viewpoints and indicate that CNOT7 has CNOT6/6L-independent functions in vivo. We also demonstrate that the mouse testis has an endogenous complex that contains CNOT7 and CNOT4, but not CNOT6/6L. CNOT4 is required for post-implantation embryo development and meiosis progression during spermatogenesis. Selective knockout of Cnot4 in male germ cells leads to defective DNA damage repair and homologous crossover formation between X and Y chromosomes in a cell autonomous manner. CNOT4 functions as a previously unrecognized mRNA adaptor of CCR4-NOT by targeting mRNAs to CNOT7 for deadenylation of the poly(A) tails, thereby mediating the degradation of a subset of transcripts from the zygotene to pachytene stage. Therefore, the mRNA removal promoted by CNOT4-regulated CCR4-NOT complex during the zygotene to pachytene transition is crucial for the selection of DNA repair pathways, subsequent activation of meiosis-related genes, sex chromosome paring, and ultimately, male fertility.

2021-02-19 | GSE158471 | GEO

RNA IP Seq analysis of Cnot7 in 4T1 mammary tumor cells

Project description:Native RNA immunoprecipitation of Cnot7-bound transcripts. Abstract: Accumulating evidence supports the role of an aberrant transcriptome as a driver of tumor cell metastatic potential. Deadenylation is a general regulatory node for post-transcriptional control by microRNAs and other determinants of RNA stability. We show here that CCR4-NOT subunit CNOT7 is a deadenylase-dependent driver of tumor cell autonomous metastatic potential. Metastasis promotion by CNOT7 is dependent on contact with CNOT1 and TOB1. We further show TOB1 independently drives metastasis. RNA-immunoprecipitation and integrated transcriptome wide analyses reveal that CNOT7-regulated transcripts are enriched for a tripartite 3’UTR motif bound by RNA-binding proteins known to complex with CNOT7, TOB1, and CNOT1. Collectively, our data support a model of CNOT7, TOB1, CNOT1, and RNA-binding proteins collectively exerting post-transcriptional control on a metastasis suppressive transcriptional program to drive tumor cell metastasis. 48 total samples, 4-5 biological replicates, two forms of control: input samples and vector controls

2015-09-23 | E-GEOD-73366 | biostudies-arrayexpress

Cnot8 Eliminates Naïve Regulation Networks and Is Essential for Naïve-to-Formative Pluripotency Transition [scRNA-Seq]

Project description:The transition of mammalian early epiblast at different phases is characterized by the differences of pluripotent states and developmental potential, involving extensive transcriptome changes. However, the role of post-transcriptional RNA degradation modulation in cell fate transition remains largely unexplored. Here, we report that deadenylase Cnot8 of Ccr4-Not complex specifically plays a role in naïve-to-formative transition of pluripotent stem cells (PSCs). Disruption of Cnot8 results in early embryonic lethality, accompanying with the increased expression levels of naïve transcription factors in mouse epiblasts. Cnot8 depletion leads to accumulated expression abundances and increased poly(A) tail lengths of massive transcripts including mRNAs of naïve regulation networks, impairing the naïve-to-formative pluripotency conversion. Mechanistically, Cnot8 interacts with Tob1 and Pabpc1 to guarantee the prompt mRNA deadenylation and degradation of naïve regulation networks at specific time. Together, these findings delineate the mechanism underlying PSC fate transition through global degradation of mRNAs for naïve regulation networks by Cnot8.

2022-05-11 | GSE194431 | GEO

Cnot8 Eliminates Naïve Regulation Networks and Is Essential for Naïve-to-Formative Pluripotency Transition (RNA-Seq)

2022-05-11 | GSE174424 | GEO

Cnot8 Eliminates Naïve Regulation Networks and Is Essential for Naïve-to-Formative Pluripotency Transition (PAIso-Seq)

2022-05-11 | GSE174423 | GEO

RNA IP Seq analysis of Cnot7 in 4T1 mammary tumor cells

2015-09-23 | GSE73366 | GEO