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PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [Stat3KO rescue]

ABSTRACT: PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [Stat3KO rescue]

PROVIDER: PRJNA851029 | ENA |

REPOSITORIES: ENA

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PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [Stat3KO rescue]

Project description:Developmental and metabolic signaling networks underpinning type-17 cell fate decisions and functional effects at coordination of PTEN-dependent tissue homeostasis

2022-10-04 | GSE206462 | GEO

PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [Raptor_or_Rictor_KO_rescue]

Project description:PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [Raptor_or_Rictor_KO_rescue]

| PRJNA851040 | ENA

PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [Raptor_or_Rictor_KO_rescue]

Project description:Developmental and metabolic signaling networks underpinning type-17 cell fate decisions and functional effects at coordination of PTEN-dependent tissue homeostasis

2022-10-04 | GSE206467 | GEO

PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [scRNA-seq and scTCR-seq Exp2]

Project description:PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [scRNA-seq and scTCR-seq Exp2]

| PRJNA851033 | ENA

Metabolic reprogramming of innate-like T cell fate and tissue homeostasis by PTEN [scRNA- and scTCR-seq]

Project description:Metabolic reprogramming of innate-like T cell fate and tissue homeostasis by PTEN [scRNA- and scTCR-seq]

| PRJNA744086 | ENA

The basic leucine zipper transcription factor NFIL3 directs the development of a common innate lymphoid cell precursor

Project description:Innate lymphoid cells (ILCs) are recently identified lymphocytes that limit infection and promote tissue repair at mucosal surfaces. However, the pathways underlying ILC development remain unclear. Here we show that the transcription factor NFIL3 directs the development of a committed bone marrow precursor that differentiates into all known ILC lineages. NFIL3 was required in the common lymphoid progenitor (CLP), and was essential for the differentiation of CLP, a bone marrow cell population that gives rise to all known ILC lineages. Clonal differentiation studies revealed that CXCR6+ cells within the CLP population differentiate into all ILC lineages but not T- and B-cells. We further show that NFIL3 governs ILC development by directly regulating expression of the transcription factor TOX. These findings establish that NFIL3 directs the differentiation of a committed ILC precursor that gives rise to all ILC lineages and provide insight into the defining role of NFIL3 in ILC development. This experiment is to compare gene expression profiles between wild-type and Nfil3-/- common lymphoid progenitor (CLP) cells to identify genes regulated by NFIL3. There are 6 samples in this experiment, including 3 biological replicates for wild-type CLPs and 3 biological replicates for Nfil3-/- CLPs. All mice used are on the C57BL/6 background.

2014-10-16 | E-GEOD-62337 | biostudies-arrayexpress

PLEKHS1 drives PI3Ks and remodels pathway homeostasis in PTEN-null prostate

Project description:The PIP3/PI3K network is a central regulator of metabolism and is frequently activated in cancer, commonly by loss of the PIP3/PI(3,4)P2-phosphatase, PTEN. Despite huge investment, the drivers of the PI3K network in normal tissues and how they adapt to overactivation are unclear. We find that in healthy mouse prostate PI3K activity is driven by RTK/IRS signalling and constrained by pathway-feedback. In the absence of PTEN, the network is dramatically remodelled. A poorly understood, YXXM- and PIP3/PI(3,4)P2-binding PH domain-containing, adaptor, PLEKHS1, became the dominant activator and was required to sustain PIP3, AKT-phosphorylation and growth in PTEN-null prostate. This was because PLEKHS1 evaded pathway-feedback and experienced enhanced PI3K- and SRC-family kinase-dependent phosphorylation of Y258XXM, eliciting PI3K-activation. hPLEKHS1-mRNA and activating-Y419-phosphorylation of hSRC correlated with PI3K-pathway activity in human prostate cancers. We propose that in PTEN-null cells, receptor-independent, SRC-dependent tyrosine-phosphorylation of PLEKHS1 creates positive-feedback that escapes homeostasis, drives PIP3-signalling and supports tumour progression.

2023-08-23 | PXD043239 | Pride

PTEN directs developmental and metabolic signaling for innate-like T cells fate and tissue homeostasis [scRNA-seq and scTCR-seq Exp2]

Project description:Developmental and metabolic signaling networks underpinning type-17 cell fate decisions in dictating tissue homeostasis versus tissue homeostasis

2022-10-04 | GSE206458 | GEO

Thymic development of type-17 innate-like T cells depends on PTEN

Project description:Thymic development of type-17 innate-like T cells depends on PTEN

| PRJNA744084 | ENA

Thymic development of type-17 innate-like T cells depends on a PTEN-coordinated two-step process linking TCR and IL-23–IL-23R–Stat3 axis

Project description:PTEN orchestrates a two-step process downstream of TCR and IL-23–Stat3 signaling to control type-17 innate-like T cell generation. Complete or partial deletion of PTEN led to the massive and selective accumulation of IL-17-producing thymocytes We used microarrays to compare the global transcription profiles of WT, Cd4CrePtenfl/fl, and Cd4CrePten+/fl thymocyte population

2022-10-04 | GSE152294 | GEO

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