MALGENEXPRESSION

The role of a nuclear expression site in the regulation of virulence genes in malaria parasites

Coordinatore	THE HEBREW UNIVERSITY OF JERUSALEM.    more  Organization address address: GIVAT RAM CAMPUS city: JERUSALEM postcode: 91904 contact info Titolo: Dr. Nome: Eran Cognome: Vardi Email: send email Telefono: -6585706 Fax: -6512235
Nazionalità Coordinatore	Israel [IL]
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-2007-4-3-IRG
Funding Scheme	MC-IRG
Anno di inizio	2008
Periodo (anno-mese-giorno)	2008-01-01   -   2011-12-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	THE HEBREW UNIVERSITY OF JERUSALEM.  Organization address address: GIVAT RAM CAMPUS city: JERUSALEM postcode: 91904 contact info Titolo: Dr. Nome: Eran Cognome: Vardi Email: send email Telefono: -6585706 Fax: -6512235	IL (JERUSALEM)	coordinator	0.00

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 Obiettivo del progetto (Objective)

'The deadliest form of human malaria is caused by the protozoan parasite, Plasmodium falciparum, which annually infects millions worldwide. The virulence of P. falciparum is attributed to its ability to evade the human immune system, by modifying the host red blood cell surface to adhere to the vascular endothelium and to undergo antigenic variation. The main cell surface ligands responsible for both cytoadherence and antigenic variation are members of the P. falciparum Erythrocyte Membrane Protein-1 (PfEMP1) family. These polymorphic proteins are encoded by a multi-copy gene family called var. Each individual parasite expresses a single var gene at a time, whereas the remaining ~60 var genes found in its genome are maintained in a transcriptionally silent state. Switches in PfEMP1 expression allow the parasite to avoid the human immune response and maintain a long-term infection. The regulation of var gene expression is therefore responsible for both immune evasion and the pathogenicity of the disease. Mutually exclusive expression and antigenic switching of var genes is epigenetically regulated at the level of transcription. This was recently demonstrated to involve chromatin modification, subnuclear localization, promoter/promoter interactions, and sterile RNAs. However, our understanding of the molecular mechanisms by which var genes are regulated is still elusive, particularly the aspects of var gene activation. I hypothesize that there exists a specific subnuclear var expression site that is involved in var gene activation. To this end the goals of the proposed research are: 1) to determine the capacity of the postulated var expression site and its role in var gene expression; 2) to determine the specificity of the expression site as a limiting factor for var gene regulation. This knowledge could lead to ways of disrupting the parasite’s ability to evade immune attack and could be exploited for the discovery of novel targets for drug and vaccine development.'