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UB-RASDisease

Financiado

The ubiquitin system in RAS driven disease

The RAS pathway is the most frequently activated signaling node in human disease. Despite intensive efforts, effective therapeutic strategies for RAS-driven disease remain daunting. Elucidation of the mechanisms of RAS activation... ver más

31/03/2023

VLAAMS INSTITUUT...

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

VIB VZW No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Ver 2 Participantes

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2023-03-31

Línea de financiación objetivo El proyecto se financió a través de la siguiente ayuda:

ERC-2017-COG: ERC Consolidator Grant

I+D

Cerrada hace 7 años

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2 Participantes

VLAAMS INSTITUUT BIOTECHNOL...

2.00M€ | Lider

MADERAS DE LLODIO

480.90K€ | Participante

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Últimas noticias

29-11-2024: IDAE En las últimas 48 horas el Organismo IDAE ha otorgado 4 concesiones

29-11-2024: ECE En las últimas 48 horas el Organismo ECE ha otorgado 2 concesiones

29-11-2024: CMVAMADRID En las últimas 48 horas el Organismo CMVAMADRID ha otorgado 37 concesiones

Duración del proyecto: 60 meses Fecha Inicio: 2018-03-19
Fecha Fin: 2023-03-31

Líder del proyecto

VIB VZW

TRL 4-5

Presupuesto del proyecto 2M€

Descripción del proyecto The RAS pathway is the most frequently activated signaling node in human disease. Despite intensive efforts, effective therapeutic strategies for RAS-driven disease remain daunting. Elucidation of the mechanisms of RAS activation promises to lead toward novel therapeutic approaches to inhibit RAS activity, and may permit identification of patients who might benefit from RAS pathway inhibitors. Our preliminary studies show that reversible ubiquitylation controls RAS activity by altering its interaction network, thus representing a conceptually novel mechanism of RAS regulation. Our initial steps towards the understanding of the RAS ubiquitylation machinery have shown that positive regulators of RAS ubiquitylation are frequently mutated or down-regulated in RAS-driven diseases, whereas negative regulators are commonly up-regulated. These striking initial results suggest that dysregulation of RAS ubiquitylation may be an alternative mechanism that drives RAS activation in human disease. Here, we aim to elucidate the role of the ubiquitin system in RAS-driven disease. We will unravel the molecular machinery controlling RAS ubiquitylation and ascertain alterations of the identified machinery in RAS-driven disease. To assess the functional impact of these alterations, we will create genetically modified mouse models and CRISPR-engineered human cell models. We will employ cutting-edge proteomic approaches to determine how disease-associated dysregulation of RAS ubiquitylation perturbs RAS interactions and signalling. Using a synthetic biologic approach, we will obtain insights into mechanisms by which ubiquitylation modulates RAS interactions. It is significant that, in contrast to the majority of known RAS regulators, the ubiquitin enzymes are druggable, which implicates them as promising targets for inhibiting RAS activity. Thus, our studies could lead to new ways of defeating RAS-driven disease.

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