Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Hepatic transcriptome phenotypes after mTORC1 activation through Tsc1 and Depdc5 mutations

ABSTRACT: We report RNA-seq results from liver tissues of control mice, liver-specific Tsc1 knockout mice, liver-specific Depdc5 knockout mice and liver-specific Tsc1/Depdc5 double knockout mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE136684 | GEO | 2020/04/14

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Hepatic transcriptome phenotypes after mTORC1 activation through Tsc1 and Depdc5 mutations

Project description:Hepatic transcriptome phenotypes after mTORC1 activation through Tsc1 and Depdc5 mutations

| PRJNA563089 | ENA

Screen mRNAs specifically regulated by mTORC1 in calvarial osteoblasts from mice

Project description:To screen mRNAs specifically regulated by mTORC1, a global mRNA expression profile in calvarial osteoblasts (OBs) from mice with or without OB-specific Tsc1 knockout was developed using microarray. Wild type (WT) or OB-specific Tsc1 knockout (KO) mice were sacrificed, with calvarial osteoblasts harvested and subjected to total RNA extraction.

2015-11-07 | E-GEOD-74781 | biostudies-arrayexpress

Transcriptomic analysis of adipocyte Tsc1 knockout mammary glands.

Project description:We report here the adipocyte-specific ablation of Tsc1 and its affects on lactation and mammary gland function. In this dataset, mammary glands from wild-type and adipocyte Tsc1 knockout mice were isolated during lactation and analysed by RNAseq. Deletion of Tsc1 is predicted to activate mTORC1 in both peripheral and mammary adipocytes. This study demonstrates that deletion of Tsc1 in adipocytes changes mammary gland histology, and function resulting in changes to breastmilk composition.

2021-05-28 | GSE175620 | GEO

Screen mRNAs specifically regulated by mTORC1 in colon epithelial cells from mice with dextran sulfate sodium (DSS)-induced experimental colitis

Project description:To screen mRNAs specifically regulated by mTORC1, a global mRNA expression profile in colon epithelial cells (CECs) from mice with or without CECs-specific TSC1 knockout (KO) was developed using microarray. Wile-type or CECs-specific TSC1 KO mice with experimental colitis were sacrificed, with CECs harvested and subjected to total RNA extraction.

2015-11-05 | E-GEOD-74674 | biostudies-arrayexpress

Tsc1 promotes the differentiation of memory CD8+ T cells via orchestrating the transcriptional and metabolic programs

Project description:Memory CD8+ T cells are an essential component of protective immunity. Signaling via mechanistic target of rapamycin (mTOR) has been implicated in the regulation of the differentiation of effector and memory T cells. However, little is understood about the mechanisms that control mTOR activity, or the effector pathways regulated by mTOR, in this process. We describe here that tuberous sclerosis 1 (Tsc1), a regulator of mTOR signaling, plays a crucial role in promoting the differentiation and function of memory CD8+ T cells in response to Listeria monocytogenes infection. Mice with specific deletion of Tsc1 in antigen-experienced CD8+ T cells evoked normal effector responses, but were markedly impaired in the generation of memory T cells and their recall responses to antigen re-exposure in a cell-intrinsic manner. Tsc1 deficiency suppressed the generation of memory-precursor effector cells (MPECs) while promoting short-lived effector cell (SLEC) differentiation. Functional genomic analysis indicated that Tsc1 coordinated gene expression programs underlying immune function, transcriptional regulation and cell metabolism. Furthermore, Tsc1 deletion led to excessive mTORC1 activity and dysregulated cellular metabolism including glycolytic and oxidative metabolism. These findings establish a Tsc1-mediated checkpoint in linking immune signaling and cell metabolism to orchestrate memory CD8+ T cell development and function. We used microarrays to explore the gene expression profiles differentially expressed in OVA-specific CD8+ T-cells from wild-type (WT; Tsc1-fl/fl and cre-negative) and Tsc1-/- (Tsc1-fl/fl and Granzyme B-cre-positive) mice

2014-09-20 | E-GEOD-61591 | biostudies-arrayexpress

Screen mRNAs specifically regulated by mTORC1 in calvarial osteoblasts from mice

2015-11-07 | GSE74781 | GEO

Tsc1 and Vhl loss cooperates to drive renal cell carcinoma through augmenting HIF1 and NRF2 signaling pathways

Project description:Besides the truncal VHL mutations, ccRCC is characterized by upregulated MTOR signals from both preclinical and clinical studies. To understand how upregulated MTOR signals cooperate with VHL loss in promoting kidney tumorigenesis, we generated kidney-specific deletion of Vhl and Tsc1 (Vhl;Tsc1 cDKO) in mice. The mice showed decreased life span with maximal age of 11 weeks, bilateral polycystic kidney diseases from ~3 weeks and multifocal solid renal cell carcinoma with eosinophilic cytoplasm and grade 2-3 from 7 weeks old. The mouse tumors resemble histology of the human kidney tumors with VHL and TSC1 mutations. To understand the mechanism of how Tsc1 loss cooperates with Vhl loss in promoting tumorigenesis, we performed transcriptomic, metabolomic and immunohistochemical profilings of renal cortices from age-matched wild-type, Vhl or Tsc1 single knockout, and Vhl;Tsc1 cDKO mice. Tsc1 loss cooperates with Vhl loss by augmenting the HIF1 transcriptional output, as well as altering the glutamine/glutamate metabolism, urea cycle, glycogen metabolism, and activating NRF2 signaling pathways which reprogram the cells to counteract the high oxidative stress associated with the proliferation. Our study reports a ccRCC mouse model recapitulating human ccRCC with same genetic background, provides mechanistic insights concerning cooperation between upregulated mTORC1 signals and VHL loss, generates in vivo reagents for studying ccRCC, and implicates potential clinical values.

2022-05-01 | GSE131735 | GEO

Tumor Suppressor TSC1 Negatively Regulates Polo-like Kinase Expression and Controls the Balance of Schwann Cell Proliferation and Differentiation

Project description:Activation of mTOR signaling by Tsc1 ablation during early developmental stages increases SC proliferation and delays radial sorting, while causing hypomyelination in the PNS. However, knockout Tsc1 in myelinating SCs at postnatal stages promotes myelin overgrowth and outfoldings. Sustained mTOR pathway leads to activation of the PLK signaling pathway. mTOR attenuation or pharmacological inhibition of PLK1 could partially rescue myelination defects in Tsc1 mutant sciatic nerves. Our data suggest that TSC1-mTOR maintains the homeostasis of SC proliferation and differentiation in a stage-specific manner.

2018-09-05 | GSE103957 | GEO

Screen mRNAs specifically regulated by mTORC1 in colon epithelial cells from mice with dextran sulfate sodium (DSS)-induced experimental colitis

2015-11-05 | GSE74674 | GEO

Tuberous sclerosis complex 1 (Tsc1) enforces quiescence of naive T cells to promote immune homeostasis and function

Project description:The mechanisms that regulate T cell quiescence are poorly understood. We report that tuberous sclerosis complex 1 (Tsc1) establishes a quiescent program in naïve T cells by controlling cell size, cell cycle entry, and responses to T cell receptor stimulation. Loss of quiescence predisposed Tsc1-deficient T cells to apoptosis that depleted conventional T cells and invariant natural killer T cells. Loss of Tsc1 function dampened in vivo immune responses to bacterial infection. Tsc1-deficient T cells exhibited increased mTORC1 but diminished mTORC2 activities, with mTORC1 activation essential for the disruption of immune homeostasis. Therefore, Tsc1-dependent control of mTOR is crucial in establishing naïve T cell quiescence to facilitate adaptive immune function. Naïve CD4 and CD8 T cells from wild-type and Tsc1-deficient mice (in triplicates each group) were stimulated with or without TCR signaling. RNA was analyzed by microarrays. WT/KO for 0 and 4 hr for CD4 (triplicates), and WT/KO for 0 hr for CD8 (duplicates).

2011-07-11 | E-GEOD-29797 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data