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REGUNMNAT1

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NAD synthesizing enzyme NMNAT1 as a fine regulator of the survival of neuron

We propose here to investigate the role of the nuclear NAD-synthesising enzyme nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1) as a fine regulator of neuron survival, aiming at identifying new targets for intervention i... ver más

30/09/2016

THE UNIVERSITY OF...

231K€

Presupuesto del proyecto: 231K€

Líder del proyecto

THE UNIVERSITY OF NOTTINGHAM No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2016-09-30 No tenemos la información de la convocatoria

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1 Participantes

THE UNIVERSITY OF NOTTINGHAM

0.00€ | Lider

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Líder del proyecto

THE UNIVERSITY OF NOTTINGHAM No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 231K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto We propose here to investigate the role of the nuclear NAD-synthesising enzyme nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1) as a fine regulator of neuron survival, aiming at identifying new targets for intervention in age-associated pathological conditions of the nervous system. NAD synthesis is central to neuron maintenance and to the action of enzymes such as sirtuins (SIRTs), poly(ADP-ribose)polymerases (PARPs), NAD glycohydrolases and ADP-ribose cyclases, involved, via gene transcription or by signalling mechanisms, in the regulation of cell and organism lifespan, in the response of neurons to stress and in protection in models of neurodegenerative diseases. NMNAT’s involvement in these processes is rapidly emerging but has not been investigated in detail. Our preliminary studies indicate that nuclear isozyme NMNAT1 is required for neuron maintenance. Building on this, here we will test the hypothesis that NMNAT1 controls neuron survival by regulating the activity of downstream enzyme SIRT1. This project is based on the unique availability to the host laboratory of Nmnat1 genetically modified mice and on the perfect match between the expertise of the host laboratory and the complementary skills of the IEF applicant, Dr Jessica De Ingeniis, a talented researcher who has received extensive training in NAD biochemistry and metabolomics in Italy and USA. This study, which can only be accomplished by combining these skills of the IEF fellow with the mouse genetics and neurobiology expertise of the supervisor, will serve two crucial purposes. It will provide vital insights into the mechanisms of neuronal survival and the role of nuclear NAD biosynthesis, constituting a fundamental prelude to the development of specific inhibitors and activators of NMNAT1 with a pharmaceutical application; and it will fill important gaps in the competences of the IEF fellow representing a crucial, final step into the development of her independent research career.

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