Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA127325 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Aberrant activation of the mammalian target of rapamycin (mTOR) complex 1 (mTORC1) is a common molecular event in a large variety of pathological settings, including genetic tumor syndromes, cancer, and obesity. However, the cell intrinsic consequences of mTORC1 activation remain poorly defined. Here, we identify global trancriptional changes in TSC1 and TSC2 null MEFs, which exhibit constitutive activation of mTORC1, compared to wild-type littermate control lines. A rapamycin time course is included to determine those changes that are dependent on mTORC1 signaling, revealing mTORC1 induced and repressed transcripts. In order to identify mTORC1-dependent transcriptional changes, we compared wild-type MEFs to both Tsc1-/- and Tsc2-/- MEFs following serum starvation, where mTORC1 signaling is off in wild-type cells and fully active in TSC-deficient cells. All cell lines were serum-starved for 24 h, and the Tsc1-/- and Tsc2-/- cells were treated with a time course of rapamycin prior to the isolation of mRNA for microarray analysis.
2010-07-30 | GSE21755 | GEO
Project description:Aberrant activation of the mammalian target of rapamycin (mTOR) complex 1 (mTORC1) is a common molecular event in a large variety of pathological settings, including genetic tumor syndromes, cancer, and obesity. However, the cell intrinsic consequences of mTORC1 activation remain poorly defined. Here, we identify global trancriptional changes in TSC1 and TSC2 null MEFs, which exhibit constitutive activation of mTORC1, compared to wild-type littermate control lines. A rapamycin time course is included to determine those changes that are dependent on mTORC1 signaling, revealing mTORC1 induced and repressed transcripts. In order to identify mTORC1-dependent transcriptional changes, we compared wild-type MEFs to both Tsc1-/- and Tsc2-/- MEFs following serum starvation, where mTORC1 signaling is off in wild-type cells and fully active in TSC-deficient cells. All cell lines were serum-starved for 24 h, and the Tsc1-/- and Tsc2-/- cells were treated with a time course of rapamycin prior to the isolation of mRNA for microarray analysis. Immortalized wild-type (Tsc2+/+ p53-/-), Tsc1-/- (p53+/+, 3T3-immortalized), and Tsc2-/- (p53-/-, derived from a littermate of the wild-type cell line) MEFs are the three cell lines used in this study and were derived in the laboratory of David J. Kwiatkowski (Brigham and Women's Hospital, Harvard Medical School, Boston, MA). Wild-type and null MEFs were grown to 70% confluence in 10 cm plates and were serum starved for 24 h in the presence of vehicle (DMSO) for 24 h or rapamycin (20 nM) for 2, 6, 12, or 24 h. All vehicle-treated samples (0 h time points) were plated in triplicate and all rapamycin time course samples were plated in duplicate. For each replicate, expression analysis was performed by hybridization to an Affymetrix Mouse 430_2 oligonucleotide microarray chip.
2010-07-30 | E-GEOD-21755 | biostudies-arrayexpress
Project description:SM014 - SARS MA15 wild type, and SARS nsp16 mutant virus infections of C57BL6 mice - A time course
2020-03-31 | E-GEOD-49263 | ExpressionAtlas
Project description:SM012 - SARS MA15 wild type, and SARS deltaORF6 mutant virus infections of C57BL6 mice - A time course
2020-03-31 | E-GEOD-49262 | ExpressionAtlas
Project description:Transcription profiling by array of mouse wild type and DNA-repair-deficient primary dermal fibroblasts after treatment with ultraviolet radiation
2014-08-16 | E-MEXP-1968 | ExpressionAtlas
Project description:Transcription profiling by array of wild type, K-ras mutant, Wt1-null, and double K-ras mutant/Wt1-null mouse embryonic fibroblasts
2014-07-03 | E-GEOD-15325 | ExpressionAtlas
Project description:There are three projects including AE155LQ, RE161LQ, RE235LQ. AE155LQ is about the proteomes of wild type cells (WT) and E. coli RelA* OE strain during exponential growth in glucose cAA medium. E1 & E2 corresponds to the wild type cells (two biological replicate samples) and E3 & E4 corresponds to RelA* OE data (two biological replicate samples). RE161LQ is about the time-course proteome of wild type (four samples including WT_0, WT_20, WT_40 and WT_80) vs relA-deficient strain (relA_0, relA_1.5 h, relA_3 h and relA_4.5 h) during AA downshift. RE235Q is about the time-course proteome of wild type (three samples including WT_0, WT_60, WT_160) vs relA-deficient strain (three samples including relA_0, relA_60 and relA_160) during carbon downshift.
2023-01-26 | PXD035675 | Pride
Project description:Tuberous Sclerosis Complex (TSC) is caused by germline TSC1 or TSC2 mutations, leading to hyperactivation of mechanistic target of rapamycin complex 1 (mTORC1) and tumors in multiple organs including the brain, heart, lung (lymphangioleiomyomatosis), and kidney (angiomyolipoma and renal cell carcinoma). Previously, we found that TFEB is constitutively active in models of TSC. To determine the impact of TFEB in vivo, we generated two novel mouse models of TSC, resulting in premature death, in which kidney pathology was the primary phenotype. RNA sequencing revealed that lysosomal and proteasomal gene pathways were the most highly upregulated in the TSC2-deficient kidneys. Knockout of TFEB rescued both kidney pathology and overall survival in both models, indicating that TFEB is the primary driver of renal disease in TSC. Importantly, mTORC1 activity, which was elevated in the TSC2 knockout kidneys, was normalized by TFEB knockout. Knockdown of Rheb or treatment of TSC2-deficient cells with Rapamycin paradoxically increases TFEB phosphorylation at the mTORC1-site (S211) and relocalizes TFEB from the nucleus to the cytoplasm via a Rag-dependent mechanism. Accordingly, treatment of TSC2 knockout mice with Rapamycin normalized lysosomal gene expression, similar to TFEB knockout, suggesting that the beneficial effects of Rapamycin in TSC are TFEB-dependent. These results change the view of the mechanisms leading to mTORC1 hyperactivation in TSC and may lead to novel therapeutic avenues for the treatment of TSC.
2023-09-28 | GSE244072 | GEO
Project description:Transcription profiling by array of mouse embryonic fibroblasts from p27 -/- knockouts and wild-type controls to study the role of p27 in regulating the cell cycle
2014-07-25 | E-MTAB-2790 | ExpressionAtlas
Project description:Transcription profiling of murine J1 embryonic stem cells undergoing a differentiation time course to study changes in transcription during stem cell differentiation
2014-08-05 | E-GEOD-3749 | ExpressionAtlas