AID AND BEYOND

AID in adaptive immunity and beyond

 Coordinatore FUNDACAO CALOUSTE GULBENKIAN 

 Organization address address: AVENIDA DE BERNA 45A
city: LISBOA
postcode: 1000

contact info
Titolo: Prof.
Nome: António
Cognome: Coutinho
Email: send email
Telefono: -214407550
Fax: -214410501

 Nazionalità Coordinatore Portugal [PT]
 Totale costo 100˙000 €
 EC contributo 100˙000 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-IRG-2008
 Funding Scheme MC-IRG
 Anno di inizio 2008
 Periodo (anno-mese-giorno) 2008-12-01   -   2012-11-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    FUNDACAO CALOUSTE GULBENKIAN

 Organization address address: AVENIDA DE BERNA 45A
city: LISBOA
postcode: 1000

contact info
Titolo: Prof.
Nome: António
Cognome: Coutinho
Email: send email
Telefono: -214407550
Fax: -214410501

PT (LISBOA) coordinator 100˙000.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

immunoglobulin    adaptive    introduce    immunity    cytidine    lesions    csr    aid    dna    somatic   

 Obiettivo del progetto (Objective)

'This proposal revolves around the enzyme Activation-Induced Deaminase (AID). AID plays a pivotal role in adaptive immunity because it is essential to introduce the lesions in the immunoglobulin genes that ultimately lead to somatic hypermutation (SHM), class switch recombination (CSR) and immunoglobulin gene conversion (Ig GC). However, its mutagenic ability has a pernicious side effect and AID has been implicated in B lymphomas and other neoplasias. Finally, because AID belongs to a family of cytidine deaminases including members with anti-retroviral properties due to their targeting of viral cDNA, cytidine deamination of DNA is yet another unforeseen link between innate and adaptive immunity. Here, I plan to use classical molecular approaches and genetically engineered mice to discover AID co-factors for CSR, to address the rules governing AID targeting to the immunoglobulin loci and to establish murine models to evaluate the impact of ectopic expression of AID. In addition, I describe how a functional assay I developed previously to characterize orthologous AID forms can be adapted to clone molecules from distant species able to introduce lesions in DNA, with the goal of better elucidating the evolution of somatic DNA modification.'

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