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Tet2 is required for Socs activation in immune response cells [RRBS]

ABSTRACT: Tet2 is required for Socs activation in immune response cells [RRBS]

PROVIDER: PRJNA506382 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8225340_1.fastq.gz	Fastqsanger.gz
	SRR8225340_2.fastq.gz	Fastqsanger.gz
	SRR8225341_1.fastq.gz	Fastqsanger.gz
	SRR8225341_2.fastq.gz	Fastqsanger.gz
	SRR8225342_1.fastq.gz	Fastqsanger.gz

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Tet2 is required for Socs activation in immune response cells

Project description:Tet2 is required for Socs activation in immune response cells

| PRJNA506008 | ENA

Tet2 is required for Socs activation in immune response cells [RNA-seq_mouse]

Project description:Tet2 is required for Socs activation in immune response cells [RNA-seq_mouse]

| PRJNA506014 | ENA

Tet2 is required for Socs activation in immune response cells [ChIP-seq]

Project description:Tet2 is required for Socs activation in immune response cells [ChIP-seq]

| PRJNA506034 | ENA

Tet2 is required for Socs activation in immune response cells [RNA-seq_human]

Project description:Tet2 is required for Socs activation in immune response cells [RNA-seq_human]

| PRJNA506012 | ENA

Tet2 is required for Socs activation in immune response cells [RRBS]

Project description:Purpose: We have previously established an in vitro murine model that recapitulates the transformed phenotype of primary Tet2-/- mast cells expressing the Kit kinase domain mutant allele, D816V, that is both an oncogene and characterises patients with mastocytosis. To better understand the molecular basis of this cooperation and to further our understanding of role of Tet2 during inflammation and in other immune system disorders, we used this same in vitro primary cell system for genome wide studies to identify genes and genomic loci that are deregulated when these two mutations cooperate in mast cells.

2020-12-31 | GSE122797 | GEO

Tet2 is required for Socs activation in immune response cells [RNA-seq_mouse]

2020-12-31 | GSE122684 | GEO

Tet2 is required for Socs activation in immune response cells [ChIP-seq]

2020-12-31 | GSE122700 | GEO

Tet2 is required for Socs activation in immune response cells [RNA-seq_human]

Project description:Purpose: Systemic mastocytosis is a rare and chronic disease with phenotypes ranging from indolent to severe. Prognosis for this disease is variable and very few biomarkers to predict disease evolution or outcome are currently known. We have performed comprehensive screening in our large cohort of systemic mastocytosis patients for mutations previously found in other myeloid diseases and that could serve as prognostic indicators. KIT, SRSF2-P95 and TET2 mutations were by far the most frequent, detected in 81, 24 and 21 percent of patients, respectively. To understand the molecular mechanisms that regulate the functional cooperation that we and others have described for oncogenic KitD816V and Tet2 loss-of-function mutations in aggressive mastocytosis, and as part of a larger study, we have sequenced the transcriptomes of mast cells sorted from bone marrow biopsies of 3 patients in our cohort with aggressive disease and KitD816V mutation and 3 patients with aggressive disease, KitD816V and Tet2 mutation.

2020-12-31 | GSE122685 | GEO

RRBS of TET2-mutant human neutrophils

Project description:RRBS of TET2-mutant human neutrophils

| PRJNA882416 | ENA

SOCS-3 in muscle

Project description:Aims/hypothesis Due to their ability to regulate various signalling pathways (cytokines, hormones, growth factors), the suppressor of cytokine signalling (SOCS) proteins are thought to be promising therapeutic targets for metabolic and inflammatory disorders. Hence, their role in vivo has to be precisely determined. Methods We generated transgenic mice constitutively expressing SOCS-3 in skeletal muscle to define whether the sole expression of SOCS-3 is sufficient to induce metabolic disorders and whether SOCS-3 is implicated in physiological roles distinct from metabolism. Results We demonstrate here that chronic expression of SOCS-3 in skeletal muscle leads to overweight in mice and worsening of high-fat diet-induced systemic insulin resistance. Counter intuitively, insulin sensitivity in muscle of transgenic mice appears to be unaltered. However, following constitutive SOCS-3 expression, several genes had deregulated expression, among them other members of the SOCS family. This could maintain the insulin signal into skeletal muscle. Interestingly, we found that SOCS-3 interacts with calcineurin, which has been implicated in muscle contractility. In SOCS-3 transgenic muscle, this leads to delocalisation of calcineurin to the fibre periphery. Relevant to this finding, SOCS-3 transgenic animals had dilatation of the sarcoplasmic reticulum associated with swollen mitochondria and decreased voluntary activity. Conclusions/interpretation Our results show that constitutive SOCS-3 expression in skeletal muscle is not in itself sufficient to induce the establishment of metabolic disorders such as diabetes. In contrast, we reveal a novel role of SOCS-3, which appears to be important for muscle integrity and locomotor activity. (Patricia Lebrun et al, Diabetologia, 2009)

2009-12-31 | GSE17063 | GEO

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