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Mechanisms for the selective clearance of chemically damaged proteins in mammali...

Mechanisms for the selective clearance of chemically damaged proteins in mammalian cells Cellular homeostasis and survival critically depend on the ability to remove misfolded and damaged proteins. In cells, proteins are continuously exposed to reactive metabolites which introduce modifications such as oxidation, carb... ver más

31/08/2023

ETH Zürich

191K€

Presupuesto del proyecto: 191K€

Líder del proyecto

EIDGENOESSISCHE TECHNISCHE HOCHSCHULE ZUERICH No se ha especificado una descripción o un objeto social para esta compañía.

Fecha límite participación Sin fecha límite de participación.

Ver 2 Participantes

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2023-08-31

MSCA-IF-2019: Individual Fellowships Objective:The goal of the Individual Fellowships is to enhance the creative and innovative potential...

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

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2 Participantes

ETH Zürich

191.15K€ | Lider

AUDITESA

179.32K€ | Participante

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Duración del proyecto: 37 meses Fecha Inicio: 2020-07-16
Fecha Fin: 2023-08-31

Líder del proyecto

EIDGENOESSISCHE TECHNISCHE HOCHSCHULE ZUERICH No se ha especificado una descripción o un objeto social para esta compañía.

Presupuesto del proyecto 191K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Cellular homeostasis and survival critically depend on the ability to remove misfolded and damaged proteins. In cells, proteins are continuously exposed to reactive metabolites which introduce modifications such as oxidation, carbonylation, glycation or carbamylation. Such non-enzymatic post-translational modifications (nePTM) can irreversibly block critical interaction surfaces or reactive sites and thus pose a constant threat to proteome integrity. In line with this view, levels of nePTM are increased in diseased and aged tissues. In contrast, nePTM-bearing proteins are selectively degraded in healthy cells, suggesting the existence of a so far unknown pathway that recognizes and eliminates nePTM-bearing proteins. In this project, I will study the impact of nePTMs on protein turnover and explore the underlying molecular mechanisms. More specifically, I plan to (I) establish a reporter assay to monitor the degradation of proteins displaying individual amino acid modifications in human cells. This will allow to test effects of common nePTMs and to identify the precise chemical adducts that induce protein clearance. Aim (II) is to uncover the cellular machinery that mediates nePTM-triggered protein degradation. To this end, I will perform a genome-wide CRISPR screen for genes required to eliminate a fluorescent model substrate. Aim (III) of the project is to understand the mechanisms underlying the recognition and clearance of nePTMs. I will therefore characterize one newly identified mediator of nePTM-clearance in detail and test its ability to bind, degrade or modify nePTM-bearing proteins and will study the impact of its knockout on the turnover of endogenous proteins. Together these experiments promise to uncover a novel pathway for the quality control of chemically damaged proteins which will form the basis for understanding its role in physiology and human disease.

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