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BIOID IN TLS

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Identification of novel regulators of translesion DNA synthesis in human cells

Here, I propose to unravel the molecular mechanisms that regulate TLS during DNA damage bypass through advanced complementary approaches. Thousands of DNA damaging insults are inflicted daily upon the genomes of all living cells.... ver más

31/12/2015

UCPH

221K€

Presupuesto del proyecto: 221K€

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 FP7 notifico la concesión del proyecto el día 2015-12-31 No tenemos la información de la convocatoria

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1 Participantes

UCPH

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Líder del proyecto

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

TRL 4-5

Presupuesto del proyecto 221K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Here, I propose to unravel the molecular mechanisms that regulate TLS during DNA damage bypass through advanced complementary approaches. Thousands of DNA damaging insults are inflicted daily upon the genomes of all living cells. If left unrepaired, these lesions can be life-threatening for organisms as they alter the content and organization of the genetic material. To overcome this constant challenge, cells are equipped with a global DNA damage response that impacts on diverse cellular processes to facilitate reestablishment of genome integrity. The genome is particularly vulnerable to DNA damage during DNA replication, where DNA is precisely duplicated as part of the cell division process. Translesion DNA synthesis (TLS), mediated by specialized low-fidelity DNA polymerases, is an important cellular mechanism for preventing gross chromosomal instability following DNA damage encountered during DNA replication. However, our understanding of how this is achieved at the molecular level remains surprisingly limited. First, in combination with state-of-the-art mass spectrometry facilities present at the CPR, I will set up a newly established screening method, termed BioID, for efficient, unbiased identification of novel proteins that specifically act at replication forks during TLS. Second, I will mine proteomic screens for DNA damage-regulated ubiquitylation for novel TLS-regulating factors. From these screens I will select the most promising candidate proteins for further validation and characterization of their potential roles in TLS regulation. I will study how these proteins impact on TLS by establishing cell lines capable of overexpressing or knocking down each factor, and employ these in a panel of biochemical and cell-based methods established in the host lab. This project will advance our understanding of the molecular mechanisms that control and integrate TLS activity with genome integrity maintenance.

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