Lavorgna, Alfonso (2008) Regulation of the NF-kappaB alternative pathway: implication for B cell transformation. [Tesi di dottorato] (Inedito)
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Tipologia del documento: | Tesi di dottorato |
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Lingua: | English |
Titolo: | Regulation of the NF-kappaB alternative pathway: implication for B cell transformation |
Autori: | Autore Email Lavorgna, Alfonso alfonso.lavorgna@libero.it |
Data: | 9 Dicembre 2008 |
Numero di pagine: | 46 |
Istituzione: | Università degli Studi di Napoli Federico II |
Dipartimento: | Biologia e patologia cellullare e molecolare "L. Califano" |
Scuola di dottorato: | Medicina molecolare |
Dottorato: | Oncologia ed endocrinologia molecolare |
Ciclo di dottorato: | 21 |
Coordinatore del Corso di dottorato: | nome email Vecchio, Giancarlo vecchio@unina.it |
Tutor: | nome email Leonardi, Antonio leonardi@unina.it |
Data: | 9 Dicembre 2008 |
Numero di pagine: | 46 |
Parole chiave: | NF-kappaB, TRAF1, BAFF Receptor |
Settori scientifico-disciplinari del MIUR: | Area 06 - Scienze mediche > MED/04 - Patologia generale |
Depositato il: | 06 Lug 2010 10:59 |
Ultima modifica: | 30 Apr 2014 19:39 |
URI: | http://www.fedoa.unina.it/id/eprint/4003 |
DOI: | 10.6092/UNINA/FEDOA/4003 |
Abstract
The NF-B2 gene is recurrently mutated and over-expressed in human lymphoid malignancies. However, a casual relationship between NF-B2 mutation and lymphomagenesis has not been established. It is also unclear how the mutation may lead to lymphoid malignancies. Recent studies suggest that nuclear factor B inducing kinase (NIK) is suppressed through constitutive proteasome-mediated degradation regulated by TRAF3, thus preventing processing of the NF-B2 precursor protein p100 to release p52. Here we demonstrate that BAFF Receptor, a member of the TNF Receptor family, interact with TRAF1, a member of TRAF family. This interaction activates NF-B2 via increased degradation of TRAF3 and stabilization of NIK. Indeed, interference of TRAF1 in lymphoma B cell line downregulates p100 processing and lead to decreased survival of B cells.
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