IMMUNOSWITCH

Switch recombination: a model system for DNA editing and repair in human lymphocytes with relevance for primary immunodeficiency and cancer formation

 Coordinatore KAROLINSKA INSTITUTET 

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore Sweden [SE]
 Totale costo 1˙888˙166 €
 EC contributo 1˙888˙166 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2009-StG
 Funding Scheme ERC-SG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-12-01   -   2014-11-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    KAROLINSKA INSTITUTET

 Organization address address: Nobels Vag 5
city: STOCKHOLM
postcode: 17177

contact info
Titolo: Dr.
Nome: Qiang
Cognome: Pan Hammarström
Email: send email
Telefono: -52483554
Fax: -52483550

SE (STOCKHOLM) hostInstitution 1˙888˙166.00
2    KAROLINSKA INSTITUTET

 Organization address address: Nobels Vag 5
city: STOCKHOLM
postcode: 17177

contact info
Titolo: Mr.
Nome: Kim
Cognome: Von Schoultz
Email: send email
Telefono: +46 8 52486071
Fax: +46 8 52483702

SE (STOCKHOLM) hostInstitution 1˙888˙166.00

Mappa


 Word cloud

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csr    immunodeficiency    immunoglobulin    induced    patients    mutations    dna    samples    shm    repair    assays    recombination    pathways    defect    diseases   

 Obiettivo del progetto (Objective)

The aim of this project is to try to understand the complex molecular mechanisms involved in DNA editing, repair and recombination during immunoglobulin class switch recombination (CSR) and somatic hypermutation (SHM). We have developed a series of PCR-based assays to study in vivo generated CSR junctions and the pattern of mutations introduced in the immunoglobulin variable region genes in human B cells, allowing us to characterize CSR and SHM in patients with immunodeficiency due to defect(s) in DNA repair/recombination. Novel in vitro CSR assays, based on GFP expression, allowing quantitative measurement of substrate recombination, are also being developed. In addition, we have initiated an evolutionary analysis of the function and structure of activation-induced deaminase, an essential molecule involved both in CSR and SHM, aiming to identify CSR specific-cofactor(s). Combining these approaches, we will be able to define the DNA repair pathways involved in CSR and SHM. The suggested project requires access to patients with various defects in the DNA repair pathways. Many of these diseases are exceedingly rare. However, through worldwide collaboration, we have obtained samples from a majority of the diagnosed patients. We are also refining the existing screening methods and developing novel methods, that will allow identification of additional patients both with recognized and new diseases caused by mutations in DNA repair pathways. Finally, we hope to be able to address the question whether illegitimate CSR events are associated with predisposition to lymphomagenesis in patients with immunodeficiency/DNA repair defect(s), by analyzing the CSR induced chromosomal breaks and translocations in these patients. A large-scale sequencing project is also planned to characterize the CSRnome in B-cell lymphoma samples.

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