Ontology highlight
ABSTRACT:
PROVIDER: PRJNA121031 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE18924: Expression data from the liver of wild-type and Cnot3+/- mice: Fasted GSE18925: Expression data from the liver of wild-type and Cnot3+/- mice: Fed vs Fasted Refer to individual Series
2011-12-09 | E-GEOD-18926 | biostudies-arrayexpress
Project description:Expression data from the liver of wild-type and Cnot3+/- mice: Fasted
| PRJNA123885 | ENA
Project description:Decay of mRNAs initiates with shortening of the poly(A) tail. Although the CCR4-NOT complex participates in deadenylation, how it becomes activates remain obscure. We show that complete deficiency in CNOT3, subunit 3 of this complex, is lethal in mice, but that heterozygotes survive as lean mice with hepatic and adipose tissues containing reduced lipid levels. Cnot3+/- mice have enhanced metabolic rates and remain lean on high-fat diets. To examine the underlying mechanisms by which CNOT3 is involved in the control of metabolic balance, we compared the gene expression profiles of wild-type and Cnot3+/- mice using Affymetrix microarray technology. We chose to analyze the liver because the CNOT3 level in the liver was affected by the feeding condition and because the liver plays a major role in glucose and lipid metabolism. The livers were isolated from 12-week-old wild-type and Cnot3+/- mice (n = 2 for each genotype).
2011-12-09 | E-GEOD-18924 | biostudies-arrayexpress
Project description:Decay of mRNAs initiates with shortening of the poly(A) tail. Although the CCR4-NOT complex participates in deadenylation, how it becomes activates remain obscure. We show that complete deficiency in CNOT3, subunit 3 of this complex, is lethal in mice, but that heterozygotes survive as lean mice with hepatic and adipose tissues containing reduced lipid levels. Cnot3+/- mice have enhanced metabolic rates and remain lean on high-fat diets. To examine the underlying mechanisms by which CNOT3 is involved in the control of metabolic balance, we compared the gene expression profiles of wild-type and Cnot3+/- mice using Affymetrix microarray technology. We chose to analyze the liver because the CNOT3 level in the liver was affected by the feeding condition and because the liver plays a major role in glucose and lipid metabolism.
2011-12-09 | GSE18924 | GEO
Project description:Expression data from the liver of wild-type and Cnot3+/- mice: Fed vs Fasted
| PRJNA123887 | ENA
Project description:Decay of mRNAs initiates with shortening of the poly(A) tail. Although the CCR4-NOT complex participates in deadenylation, how it becomes activates remain obscure. We show that complete deficiency in CNOT3, subunit 3 of this complex, is lethal in mice, but that heterozygotes survive as lean mice with hepatic and adipose tissues containing reduced lipid levels. Cnot3+/- mice have enhanced metabolic rates and remain lean on high-fat diets. We further provide evidence suggesting that CNOT3, by changing its level in response to feeding conditions, affects the activity of the CCR4-NOT deadenylase against poly(A) tails of specific mRNAs coding for proteins involved in metabolism of carbohydrates and fats. Because the levels of CNOT3 protein were decreased under fasting conditions and increased upon refeeding and because CNOT3 could be a positive regulator of the CCR4-NOT deadenylase, we hypothesized that the levels of CCR4-NOT target mRNAs would be lower in fed mice than in fasted mice. We compared the gene expression profiles of fed and fasted wild-type mice. Microarray analysis revealed that approximately 1,200 mRNA transcripts were down-regulated in the livers of fed mice. Of these mRNAs, 68 corresponded to the genes up-regulated in the livers of Cnot3+/- mice and fasted wild-type mice. A large number of the 68 identified genes encoded proteins involved in metabolism, especially lipid metabolism and growth. The livers were isolated from 8-week-old fed wild-type, fasted wild-type and fasted Cnot3+/- mice (n = 2 for each genotype).
2011-12-09 | E-GEOD-18925 | biostudies-arrayexpress
Project description:Decay of mRNAs initiates with shortening of the poly(A) tail. Although the CCR4-NOT complex participates in deadenylation, how it becomes activates remain obscure. We show that complete deficiency in CNOT3, subunit 3 of this complex, is lethal in mice, but that heterozygotes survive as lean mice with hepatic and adipose tissues containing reduced lipid levels. Cnot3+/- mice have enhanced metabolic rates and remain lean on high-fat diets. We further provide evidence suggesting that CNOT3, by changing its level in response to feeding conditions, affects the activity of the CCR4-NOT deadenylase against poly(A) tails of specific mRNAs coding for proteins involved in metabolism of carbohydrates and fats. Because the levels of CNOT3 protein were decreased under fasting conditions and increased upon refeeding and because CNOT3 could be a positive regulator of the CCR4-NOT deadenylase, we hypothesized that the levels of CCR4-NOT target mRNAs would be lower in fed mice than in fasted mice. We compared the gene expression profiles of fed and fasted wild-type mice. Microarray analysis revealed that approximately 1,200 mRNA transcripts were down-regulated in the livers of fed mice. Of these mRNAs, 68 corresponded to the genes up-regulated in the livers of Cnot3+/- mice and fasted wild-type mice. A large number of the 68 identified genes encoded proteins involved in metabolism, especially lipid metabolism and growth.
2011-12-09 | GSE18925 | GEO
Project description:Expression data from liver samples of wild type and Pfn2-/- mice
| PRJNA263905 | ENA
Project description:Expression data from wild-type mice starved as compared to wild-type control mice
| PRJNA153463 | ENA
Project description:To study the role Cnot3 in early B cells development, RNASeq analysis of pro-B cells (B220+ and CD43+) was performed in tamoxifen treated Cnot3(fl/fl) RERTCre and Cnot3+/+;RERTCre mice.
2016-11-21 | GSE87635 | GEO