NOSTRESS
Unraveling the molecular mechanism of nitrosative stress resistance in tuberculosis
| Coordinatore |
Organization address
address: GRAN VIA DE LES CORTS CATALANES 585 contact info |
| Nazionalità Coordinatore | Non specificata |
| Totale costo | 1˙540˙956 € |
| EC contributo | 0 € |
| Programma | FP7-HEALTH
Specific Programme "Cooperation": Health |
| Anno di inizio | 2008 |
| Periodo (anno-mese-giorno) | 2008-10-01 - 2012-03-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
UNIVERSITAT DE BARCELONA
Organization address
address: GRAN VIA DE LES CORTS CATALANES 585 contact info |
ES (BARCELONA) | coordinator | 0.00 |
| 2 |
AGENCIA ESTATAL CONSEJO SUPERIOR DE INVESTIGACIONES CIENTIFICAS
Organization address
address: CALLE SERRANO 117 contact info |
ES (MADRID) | participant | 0.00 |
| 3 |
COUNCIL OF SCIENTIFIC AND INDUSTRIAL RESEARCH
Organization address
address: Anusandhan Bhawan, Rafi Marg 2 contact info |
IN (NEW DEHLI) | participant | 0.00 |
| 4 |
THE UNIVERSITY OF SHEFFIELD
Organization address
address: FIRTH COURT WESTERN BANK contact info |
UK (SHEFFIELD) | participant | 0.00 |
| 5 |
UNIVERSIDAD DE BUENOS AIRES
Organization address
address: Viamonte 430/444 contact info |
AR (BUENOS AIRES) | participant | 0.00 |
Mappa
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Obiettivo del progetto (Objective)
'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.'
Introduzione (Teaser)
Tuberculosis remains a major health problem worldwide, with over two million deaths every year and one billion latently infected individuals. Current treatments are hampered by multidrug-resistant strains, drug side effects, and co-infections, necessitating the prompt identification of potent, safe anti-mycobacterial agents.
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