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XlinkRepair

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Understanding DNA interstrand crosslink repair the Fanconi anemia pathway and...

Understanding DNA interstrand crosslink repair the Fanconi anemia pathway and beyond DNA interstrand crosslinks (ICLs) are toxic DNA lesions that are induced by cancer chemotherapeutics but are also formed endogenously. ICL repair is mostly linked to DNA replication, which complicated the biochemical dissection of... see more

30/04/2026

KNAW

2M€

Project Budget: 2M€

Project leader

KONINKLIJKE NEDERLANDSE AKADEMIE VAN WETENSCH... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

PARTICIPATION DEPralty Sin fecha límite de participación.

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Financing granted El organismo H2020 notifico la concesión del proyecto The day 2021-01-27

ERC-2020-COG: ERC CONSOLIDATOR GRANTS Scope:Objectives

I+D

Cerrada does 5 years

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Este proyecto no cuenta con búsquedas de partenariado abiertas en este momento.

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2 Participantes

KNAW

2.00M€ | Leader

LPG TECNICAS EXTINCION INCEN...

283.24K€ | participant

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Project duration: 63 months Date Start: 2021-01-27
End date: 2026-04-30

Project leader

KONINKLIJKE NEDERLANDSE AKADEMIE VAN WETENSCH... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Project Budget 2M€

participation deadline Sin fecha límite de participación.

Project description DNA interstrand crosslinks (ICLs) are toxic DNA lesions that are induced by cancer chemotherapeutics but are also formed endogenously. ICL repair is mostly linked to DNA replication, which complicated the biochemical dissection of this process. The classical ICL repair pathway is the Fanconi anemia pathway, affected in the cancer predisposition syndrome Fanconi anemia (FA). Although the repair mechanism is poorly understood, recent studies have revealed unanticipated insights that now allow us to address key questions. While the FA pathway was long thought to be the only replication-coupled ICL repair pathway, two novel pathways were recently discovered. We described one novel pathway that repairs endogenous ICLs induced by acetaldehyde, a product of alcohol metabolism. However, mechanistic details of this novel pathway are lacking. Other unexplored aspects are the role of the chromatin context and the mutagenic consequences of repair. Here, I will capitalize on my group’s expertise applying a unique biochemical system that recapitulates ICL repair, and combine this with newly developed tools to address these objectives: 1) We will decipher key steps in the FA pathway of ICL repair. We will resolve the roles(s) of the FA core complex and the direct function of FANCI-FANCD2 ubiquitination, a key activating step. 2) We will move into new directions and investigate FA-independent ICL repair pathways. We will determine the molecular mechanism of acetaldehyde ICL repair and investigate the repair mechanisms of other aldehyde-induced ICLs. 3) We will extend our knowledge beyond the direct repair factors by defining chromatin dynamics during ICL repair and determining its role. In addition, we will delineate the mutagenicity of ICL repair to evaluate its consequences. These studies will provide important novel insights into how cells maintain genome integrity, increase our understanding of Fanconi anemia, and may improve strategies in chemotherapeutic treatment.

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