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NOSTRESS

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Unraveling the molecular mechanism of nitrosative stress resistance in tuberculo...

Unraveling the molecular mechanism of nitrosative stress resistance in tuberculosis Tuberculosis is today amongst the major worldwide health threats. Treatment failure is unfortunately becoming more usual, especially in countries lacking the long and costly treatment adapted to patients. Thus, tuberculosis causes... ver más

31/03/2012

2M€

Presupuesto del proyecto: 2M€

Líder del proyecto

UNIVERSIDAD DE BARCELONA No se ha especificado una descripción o un objeto social para esta compañía.

Total investigadores 328

Fecha límite participación Sin fecha límite de participación.

Ver 7 Participantes

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2012-03-31 No tenemos la información de la convocatoria

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Información adicional privada

No hay información privada compartida para este proyecto. Habla con el coordinador.

7 Participantes

0.00€ | Lider

UNIVERSIDAD DE BUENOS AIRES

USFD

N.D. | Participante

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Líder del proyecto

UNIVERSIDAD DE BARCELONA No se ha especificado una descripción o un objeto social para esta compañía.

Total investigadores 328

Presupuesto del proyecto 2M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Tuberculosis is today amongst the major worldwide health threats. Treatment failure is unfortunately becoming more usual, especially in countries lacking the long and costly treatment adapted to patients. Thus, tuberculosis causes 2 million deaths every year and latently persists in over 1 billion individuals worldwide. Current treatments are challenged by multidrug resistant strains, drug side effects, and co-infections. Therefore, identification of potent, safety antimycobacterial agents is mandatory. However, the success of this strategy is largely determined by the detailed knowledge of their mechanism of action, which in turn depends on the validation of suitable biological targets. This project pursues the definition of new, complementary therapeutic approaches by identifying the molecular basis of the nitrosative stress resistance of M. tuberculosis. Our working hypothesis is that a decrease in the NO resistance of the microorganism should reduce significantly the capability to rest in latency, thus contributing to increase the efficacy of the therapeutic treatment. In this context, understanding of the NO detoxification activity played by M. tuberculosis trHbN is essential. Accordingly, our objectives are i) to unravel the molecular mechanism underlying the NO dioxygenase activity of M. tuberculosis trHbN, ii) to establish the structure-function relationships in trHbN and trHbO from M. tuberculosis, and iii) to identify the reductase protein system that helps trHbN to restore the ferrous state required to initiate the NO detoxification cycle. The outcome of the project should provide a firm basis to assess the viability of trHbN as a therapeutic target, and set up the background to exploit this knowledge in the design of innovative therapeutic strategies to fight the disease.

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