TRANSCRIPTIONALNLRS

NLRs AS TRANSCRIPTIONAL REGULATORS

 Coordinatore UNIVERSITE DE LAUSANNE 

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

 Nazionalità Coordinatore Switzerland [CH]
 Totale costo 1˙499˙154 €
 EC contributo 1˙499˙154 €
 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-2012-StG_20111109
 Funding Scheme ERC-SG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-03-01   -   2018-02-28

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITE DE LAUSANNE

 Organization address city: LAUSANNE
postcode: 1015

contact info
Titolo: Dr.
Nome: Greta
Cognome: Guarda
Email: send email
Telefono: +41 21 6925708
Fax: +41 21 6925705

CH (LAUSANNE) hostInstitution 1˙499˙154.00
2    UNIVERSITE DE LAUSANNE

 Organization address city: LAUSANNE
postcode: 1015

contact info
Titolo: Ms.
Nome: Natasa
Cognome: Jovanovic
Email: send email
Telefono: +41 21 6925708
Fax: +41 21 6925705

CH (LAUSANNE) hostInstitution 1˙499˙154.00

Mappa


 Word cloud

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

rfx    ciita    regulation    molecules    knockout    expression    function    play    mhcii    transcription    mhci    promoter    homologous    gene    enhanceosome    mhc    transcriptional    nlr    nlrc    plan    proximal    we    immune    mice   

 Obiettivo del progetto (Objective)

'MHC molecules are central to our immune system and are therefore also involved in several pathologies. MHCII transcription is controlled by proximal promoter sequences, which are cooperatively bound by several factors forming the ‘MHC enhanceosome’. Upon recruitment to this complex, the NLR family member CIITA promotes MHCII transcription. We recently found that our mice deficient for the NLR NLRC5 exhibit markedly reduced MHCI expression in lymphocytes. Importantly, endogenous NLRC5 occupies H-2 proximal promoter regions and drives gene transcription. We now plan to characterize novel NLR-mediated transcriptional regulatory pathways controlling MHC expression. We will investigate the enhanceosome and the transcriptional regulators interacting with NLRC5 as well as the role of NLRC5 in gene expression more broadly. We will also address the function of NLRC3, which is homologous to CIITA and NLRC5, by using novel conditional knockout mice. Our preliminary data indicate that conventional Nlrc3-KO mice show embryonic lethality and that NLRC3 can localize to the nucleus, supporting the hypothesis that it acts as an essential transcriptional regulator. We will therefore investigate NLRC3 function in immunity and reproduction, paying particular attention to the regulation of non-classical MHCI molecules known to play a role in embryogenesis. Interestingly, we identified RFX7, which is homologous to the enhanceosome component RFX5, as an interactor of NLRC3. Although RFX7 has been associated with leukemia development, this factor remains functionally uncharacterized, and we plan to study its role by generating knockout mice. Novel aspects of MHC transcriptional regulation are emerging, highlighting a combinatorial system wherein NLRs play a more general role than realized so far. A better understanding of the mechanisms regulating MHC transcription is fundamental to design novel therapeutic approaches relevant to immune disorders, malignancies, and infertility.'

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