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PROTEIN TYROSINE PHOSPHATASES IN METABOLIC DISEASES OXIDATION DYSFUNCTION AND...

PROTEIN TYROSINE PHOSPHATASES IN METABOLIC DISEASES OXIDATION DYSFUNCTION AND THERAPEUTIC POTENTIAL Diabetes mellitus is characterised by hyperglycaemia caused by an absolute or relative insulin deficiency. The global prevalence of diabetes has reached more than 410 million individuals, underscoring the need for novel therapeuti... ver más

31/03/2025

ULB

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

UNIVERSITE LIBRE DE BRUXELLES 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 2019-03-25

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

ERC-2018-COG: ERC Consolidator Grant

I+D

Cerrada hace 6 años

0% 100%

2 Participantes

ULB

1.97M€ | Lider

VELLSAM MATERIAS BIOACTIVAS....

345.57K€ | 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: 72 meses Fecha Inicio: 2019-03-25
Fecha Fin: 2025-03-31

Líder del proyecto

UNIVERSITE LIBRE DE BRUXELLES

TRL 4-5

Presupuesto del proyecto 2M€

Descripción del proyecto Diabetes mellitus is characterised by hyperglycaemia caused by an absolute or relative insulin deficiency. The global prevalence of diabetes has reached more than 410 million individuals, underscoring the need for novel therapeutic strategies targeting the pathology as a multi-organ disease. Protein tyrosine phosphatases (PTPs) constitute a superfamily of enzymes that dephosphorylate tyrosine-phosphorylated proteins and oppose the actions of protein tyrosine kinases. My previous studies and preliminary data suggest that PTPs act as molecular switches for key signalling events in the development of diabetes, i.e. insulin/glucose/cytokine signalling. Dysregulation of these pathways results in metabolic consequences that are cell-specific. Oxidative stress abrogates the nucleophilic properties of the PTP active site and induces conformational changes that inhibit PTP activity and prevent substrate-binding. I have recently developed an innovative proteomic approach to quantify PTP oxidation in vivo and demonstrated that this occurs in liver/pancreas under pathological conditions, including obesity and inflammation. In this proposal, I aim to fully characterise the activity and oxidation status of PTPs in dysfunctional metabolic relevant cells in obesity and diabetes. Importantly, the crucial role of PTPs make them promising candidates for the treatment of metabolic disorders. I hypothesise that specific antioxidants, diets and/or adenovirus will restore PTP function and ameliorate the metabolic deleterious defects in pre-clinical studies. Over the next 5 years, I aim to: • Identify the major oxidised PTPs in metabolic relevant tissues/cells in both obesity and diabetes. • Determine the contribution of PTP inactivation in cellular responses to metabolic signalling in human samples. • Assess the impact of tissue-specific PTP deficiency on the development of obesity and diabetes. • Test novel therapeutic approaches targeting PTPs to prevent/reverse metabolic disorders.

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