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Post transcriptional regulation of effector function in T cells by RNA binding p...

Post transcriptional regulation of effector function in T cells by RNA binding proteins CD8+ T cells are critical to fight infections and to clear tumor cells through the production of inflammatory cytokines and cytotoxic molecules. These effector molecules must be tightly controlled: too little leads to the inabilit... ver más

31/08/2024

Stichting Sanquin...

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

Stichting Sanquin Bloedvoorziening No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

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Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2024-08-31

ERC-2018-COG: ERC Consolidator Grant

I+D

Cerrada hace 6 años

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No hay información privada compartida para este proyecto. Habla con el coordinador.

2 Participantes

Stichting Sanquin Bloedvoorz...

2.00M€ | Lider

TEXSA

640.28K€ | Participante

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Duración del proyecto: 66 meses Fecha Inicio: 2019-02-28
Fecha Fin: 2024-08-31

Líder del proyecto

Stichting Sanquin Bloedvoorziening No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 2M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto CD8+ T cells are critical to fight infections and to clear tumor cells through the production of inflammatory cytokines and cytotoxic molecules. These effector molecules must be tightly controlled: too little leads to the inability to control the pathogen, and too much can result in a life-threatening cytokine storm and tissue damage. While transcriptional control of effector genes is well-studied, regulation at the levels of RNA stability and translation efficiency by RNA-binding proteins (RBPs) has remained underappreciated. We recently found that several cytokines are tightly regulated through these processes, and we identified ZFP36L2 as one of the responsible RBPs. However, much is still to be learned about the underlying molecular mechanisms. Moreover, there are >1000 putative RBPs, and a systematic analysis of their regulatory activity in T cells is lacking, particularly with regard to the control of effector proteins. Here, we will use a combination of mouse genetics, and molecular and cellular biology to gain a deep understanding of the control of cytokine production by RBPs, using ZFP36L2 as a paradigm. Next, we will take a novel, highly sensitive proteomics approach to systematically identify the RBP repertoire in resting and activated primary human T cells. Complementary functional screens will identify those RBPs that control specific effectors. Selected RBPs identified in these screens will be studied in-depth to understand their roles in T cell responses to acute infection and in tumor models. Lastly, we will define how RBPs can imprint and/or maintain the killer phenotype of human CD8+ T cells. This research will significantly advance our understanding of post-transcriptional regulation of T cell effector activity, and it should help us to develop novel tools to drive effective T cell responses against pathogens and malignant cells.

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