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DNAProteinCrossRep

Financiado

Cerrado

Identification of DNA Protein Crosslink Repair Factors

DNA damage can cause mutations and genome instability and is therefore the underlying cause of many pathologies including neurodegeneration and cancer. To maintain genome integrity, cells are equipped with sophisticated pathways f... ver más

18/04/2021

UCPH

212K€

Presupuesto del proyecto: 212K€

Líder del proyecto

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

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2021-04-18

MSCA-IF-2017: Individual Fellowships

I+D

Cerrada hace 7 años

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Información adicional privada

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

1 Participantes

UCPH

212.19K€ | Lider

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Duración del proyecto: 36 meses Fecha Inicio: 2018-04-04
Fecha Fin: 2021-04-18

Líder del proyecto

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

TRL 4-5

Presupuesto del proyecto 212K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto DNA damage can cause mutations and genome instability and is therefore the underlying cause of many pathologies including neurodegeneration and cancer. To maintain genome integrity, cells are equipped with sophisticated pathways for efficient repair of the broad spectrum of lesions that frequently arise in cellular DNA. By now, most DNA repair pathways are well understood. However, dedicated mechanisms for the repair of DNA-protein crosslinks (DPCs) have only been discovered very recently and are still poorly described. This is mainly due to a lack of approaches for specifically generating DPCs. My host lab has established a cell-based system that facilitates, for the first time, the induction of genome-wide yet defined DPCs. With this system at hand, I propose a project to identify and characterise cellular responses to DPCs in both human cells and in the nematode Caenorhabditis elegans (C. elegans). I will utilize the newly established system in a CRISPR/Cas9-based genome-wide screen to identify new DPC repair factors, and subsequently characterise their roles in promoting genome stability. I will strengthen the physiological relevance of my findings by studying orthologues of selected factors in C. elegans, in order to gain insights into their tissue specificity and roles in development and organismal fitness. By combining the host lab’s strong standing within the DNA repair field and formidable know-how in the area of cell-based studies of DNA damage repair pathways with my expertise in DNA damage research in C. elegans, I will be in a unique position to critically advance our knowlegde about DPC repair. Considering that DPCs are generated by many anti-cancer drugs, it is particularly important to illuminate the underlying repair mechanisms to improve current treatment strategies. This timely and interdisciplinary project will greatly enhance my scientific and transferrable skills required to realize my long-term goal of becoming an independent group leader.

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