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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from control or CCR4b/CNOT6L-depleted cells

ABSTRACT: The stability of mRNA influences the abundance of cellular transcripts and proteins. Deadenylases play critical roles in mRNA turnover and thus are important for the regulation of arious biological events. Here, we report the identification and characterization of CCR4b/CNOT6L, which is homologous to yeast CCR4 mRNA deadenylase. We compared the expression profiles of the cellular genes between control and CCR4b/CNOT6L-depleted cells by microarray analysis Total RNAs were extracted from control or CCR4b-depleted cells. Following the isolation of RNA, all subsequent technical procedures, including quality control of RNA, labeling, hybridization, and scanning of the arrays, were performed in BIO MATRIX Research, Inc., cDNA, and biotinlabeled cRNA was synthesized according to protocols for Affymetrix array analysis. Biotin-labeled cRNAs (15 g) were hybridized to the GeneChip Mouse Genome 430 2.0 Array (Affymetrix, Santa Clara, CA). To determine the average differences for each probe set, changes were calculated by a global normalization method using Affymetrix GCOS (GeneChipOperating Software) software.

ORGANISM(S): Mus musculus

SUBMITTER: Masahiro Morita

PROVIDER: E-GEOD-31148 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from control or CCR4b/CNOT6L-depleted cells

Project description:The stability of mRNA influences the abundance of cellular transcripts and proteins. Deadenylases play critical roles in mRNA turnover and thus are important for the regulation of arious biological events. Here, we report the identification and characterization of CCR4b/CNOT6L, which is homologous to yeast CCR4 mRNA deadenylase. We compared the expression profiles of the cellular genes between control and CCR4b/CNOT6L-depleted cells by microarray analysis

2011-08-03 | GSE31148 | GEO

Expression data from 4-week-old mouse liver

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Expression data from 1-week-old mouse liver

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Expression data from embryonic day 16.5 or postnatal day 3 mouse liver

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Expression data from mouse embryonic fibroblasts

Project description:In addition to transcriptional regulation, mRNA degradation critically contributes to gene expression as shown by various biological analysis. The CCR4-NOT complex serves as a major deadenylase that initiates mRNA degradation. We used microarrays to identify CCR4-NOT targets by searching for genes specifically stablized in the absence of CNOT3, a core subunit of the CCR4-NOT complex. Primary mouse embryonic fibroblasts (MEFs) were used for RNA extraction and hybridization on Affymetrix microarrays. CNOT3-knockdown MEFs were generated by Cre-mediated somatic recombination. We treated both control and CNOT-knockdown (CNOT3KD) MEFs with a transcriptional inhibitor, actinomycin D to focus on a stability of mRNAs.

2015-09-01 | E-GEOD-67418 | biostudies-arrayexpress

Expression data from fetal hepatocytes from control or Cnot3KO E16.5 embryos treated with Actinomycin D for 0, 6 or 12h

Project description:mRNA degradation critically contributes to liver development and function. The CCR4-NOT complex serves as a major deadenylase that initiates mRNA degradation. We used microarrays to identify abnormally stabilized mRNAs in the fetal hepatocytes lacking Cnot3, a core subunit of the CCR4-NOT complex.

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Expression data from mouse embryonic fibroblasts

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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.

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Expression data from mouse white adipose tissue lacking CNOT3, a core subunit of the CCR4-NOT complex

Project description:mRNA degradation critically contributes to tissue development and function as well as transcription. The CCR4-NOT complex serves as a major deadenylase that initiates mRNA degradation. We used microarrays to identify deregulated genes in the white adipose tissues lacking CNOT3, a core subunit of the CCR4-NOT complex.

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Examination of mRNA decay rate in mature adipocytes

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