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Hepatic transcriptome phenotypes after mTORC1 activation through Tsc1 and Depdc5 mutations

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

PROVIDER: PRJNA563089 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10049333.fastq.gz	Fastqsanger.gz
	SRR10049334.fastq.gz	Fastqsanger.gz
	SRR10049335.fastq.gz	Fastqsanger.gz
	SRR10049336.fastq.gz	Fastqsanger.gz
	SRR10049337.fastq.gz	Fastqsanger.gz

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Hepatic transcriptome phenotypes after mTORC1 activation through Tsc1 and Depdc5 mutations

Project description: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.

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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

Persistent mTORC1 activation due to loss of liver tuberous sclerosis complex 1 promotes liver injury in alcoholic hepatitis.

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Peli1-mediated TSC1 ubiquitination site

Project description:Metabolic fitness of T cells is crucial for immune responses against infections and tumorigenesis. Both the T cell receptor (TCR) signal and environmental cues contribute to the induction of T cell metabolic reprogramming, but the underlying mechanism is incompletely understood. Here we identified the E3 ubiquitin ligase Peli1 as an important regulator of T cell metabolism and antitumor immunity. Peli1 ablation profoundly promotes tumor rejection, associated with increased tumor-infiltrating CD4 and CD8 T cells. The Peli1-deficient T cells display markedly stronger metabolic activities, particularly glycolysis, than wildtype T cells. Peli1 controls the activation of a metabolic kinase, mTORC1, stimulated by both the TCR signal and growth factors, and this function of Peli1 is mediated through regulation of the mTORC1-inhibitory proteins, TSC1 and TSC2. Peli1 mediates non-degradative ubiquitination of TSC1, thereby promoting TSC1-TSC2 dimerization and TSC2 stabilization. These results establish Peli1 as an important regulator of T cell metabolism and antitumor immunity and suggest a novel mechanism that controls mTORC1 activation.

2020-11-23 | PXD020734 | Pride

Investigation of miRNA expression signatures in mTORC1 -stimulated osteoarthritis

Project description:To further explain pathology of mTORC1 -stimulated osteoarthritis, we have employed whole genome microarray expression profiling as a discovery platform to identify miRNAs which involved in development of mTORC1-stimulated osteoarthritis We generated Col2a1-specific deletion of Tsc1 mice. mTORC1 induced miRNAs expression in development of osteoarthritis was measured at eight weeks after birth. Independent experiments were performed using knee joint cartilage from Col2a1Tsc1KO and control mice.

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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.

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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.

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S6K1 Phosphoproteome in Tsc1-null mouse kidney iMCD3 cells

Project description:Loss of Tsc1 in the kidneys gives rise to rapid polycystogenesis and kidney failure due to the hyperactivation of mTOR complex I (mTORC1). One of the major downstream targets of mTORC1 is S6K1, which is responsible for driving many of the effector functions of mTOR. Strikingly, the loss of S6k1 in the context of hyperactivated mTOR is sufficient to reverse the generation of polycystic kidneys. In an effort to uncover novel direct S6k1 substrates involved in the generation of cystic kidneys, we generated Tsc1-null and Tsc1/S6k1-double null murine inner medullary collecting duct (iMCD3) cell lines using CRISPR/Cas9. Using these two cell lines, we conducted a phosphoproteome screen to search for novel candidates. Using a combination of antibody-motif enrichment and metal affinity enrichment, we provide a comprehensive phosphoproteome profile between these two genotypes.

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