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

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

PROVIDER: PRJNA744086 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR15048901_1.fastq.gz	Fastqsanger.gz
	SRR15048901_2.fastq.gz	Fastqsanger.gz
	SRR15048902_1.fastq.gz	Fastqsanger.gz
	SRR15048902_2.fastq.gz	Fastqsanger.gz

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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

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 [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

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

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

2022-10-04 | GSE179511 | GEO

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

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 [Stat3KO rescue]

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

| PRJNA851029 | ENA

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

Non-apoptotic Fas signaling controls CD40 dependent mTOR activation and human B cell fate via PTEN nuclear exclusion

Project description:Defective Fas signaling causes autoimmune lymphoproliferative syndrome (ALPS). While defective apoptosis may impair negative selection and removal of autoreactive B lymphocytes, Fas transmits also non-apoptotic signals. We show herethat transient Fas ligation in CD40L-stimulated human B cells specifically decreased the mTOR axis activation without causing apoptosis. This signal modulation was absent in ALPS patients. Rather, mTOR signaling was enhanced in germinal center (GC) B cells and plasmablasts derived from a ALPS patient lymph node . Mechanistically, transient Fas engagement induced recruitment of DAXX to the activated Fas complex and nuclear exclusion of PTEN. Likewise, Fas stimulation promoted expression of transcripts like MYC and CXCR4, that regulate GC formation and fate decisions of established GC B cells. We suggest that non-apoptotic Fas signaling has a physiological impact on activated B cell fate decisions explaining the effectiveness of mTOR inhibitors in the treatment of ALPS autoimmunity.

2024-04-08 | PXD017601 | Pride

The phosphatase PTEN links platelets with immune regulatory functions of mouse T follicular helper cells

Project description:Beyond a function in hemostasis and thrombosis, platelets can regulate innate and adaptive immune responses. Hyperactive platelets are frequently associated with multiple human autoimmune diseases, yet their pathogenic functions in these diseases have not been fully established. Emerging studies show an essential function of the phosphatase and tensin homolog (PTEN) in maintenance of immune homeostasis. Here, we show that mice with platelet-specific deletion of Pten, develop age-related lymphoproliferative diseases and humoral autoimmunity not seen in wildtype animals. Platelet-specific Pten-deficient mice have aberrant T cell activation, excessive T follicular helper (Tfh) cell responses and accumulation of platelet aggregates in lymph nodes. Transferred Pten-deficient platelets are able to infiltrate into the peripheral lymphoid tissues and form more aggregates. Moreover, Pten-deficient platelets are hyperactive and overproduce multiple Tfh-promoting cytokines via activation of the PDK1/mTORC2-AKT-SNAP23 pathway. Pten-deficient platelets show enhanced interaction with CD4+ T cells and promote conversion of CD4+ T cells into Tfh cells. Our results implicate PTEN in platelet-mediated immune homeostasis, and provide evidence that hyperactive platelets function as an important mediator in autoimmune diseases using mouse models.

2021-01-01 | GSE143698 | GEO

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