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TranscriptStress

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The transcriptional response to oxidative stress

Environmental stress triggers a cellular response to promote adaptation and survival, typically through activation of stress genes. What is less appreciated is that various types of cellular stress at the same time induce widespre... ver más

30/06/2028

UCPH

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

KOBENHAVNS UNIVERSITET No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Financiación concedida El organismo HORIZON EUROPE notifico la concesión del proyecto el día 2023-01-20

ERC-2022-STG: ERC STARTING GRANTS Scope:Objectives

I+D

Cerrada hace 2 años

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Información adicional privada

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

1 Participantes

UCPH

1.50M€ | Lider

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Duración del proyecto: 65 meses Fecha Inicio: 2023-01-20
Fecha Fin: 2028-06-30

Líder del proyecto

KOBENHAVNS UNIVERSITET No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 2M€

Descripción del proyecto Environmental stress triggers a cellular response to promote adaptation and survival, typically through activation of stress genes. What is less appreciated is that various types of cellular stress at the same time induce widespread transcriptional repression at most other genes. Although such transcriptional reprogramming is common to various kinds of cellular stress, recent evidence suggests it is governed by different stress-specific mechanisms. A brief exposure to oxidative stress leads to a rapid and transient global repression of transcription. However, our current knowledge about the oxidative stress response is extremely limited. Based on our preliminary results, I hypothesise that the transcriptional response to oxidative stress involves both regulation of transcription elongation as well as termination and that these are connected to post-translational modifications of RNA polymerase II (RNAPII) itself. Here, I propose an ambitious approach to investigate the transcriptome-wide oxidative stress response in human cells and following physiologically induced oxidative stress in mice. To this end, we will use a combination of state-of-the art sequencing techniques coupled with time-resolved proteomics and a novel screening approach. Together, our work will provide important new knowledge about the transcriptional response to oxidative stress and the factors involved – in an area that is currently not well understood. Such knowledge is also crucial to understand the fundamental mechanisms allowing RNAPII to stop transcribing and restart again. Finally, we will investigate how factors involved in the transcriptional response influence transcription-associated genome instability and neuronal cell identity. This will be relevant for diseases in which oxidative stress has been implicated, such as neurological disorders and cancer.

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