Esposito, Davide (2014) Human rpL3 regulates DNA damage reponse by modulating p21(waf1/cip1) levels in a p53-independent manner. [Tesi di dottorato]

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Item Type: Tesi di dottorato
Lingua: English
Title: Human rpL3 regulates DNA damage reponse by modulating p21(waf1/cip1) levels in a p53-independent manner
Creators:
CreatorsEmail
Esposito, Davidedavide.esposito@mssn.edu
Date: 30 March 2014
Number of Pages: 66
Institution: Università degli Studi di Napoli Federico II
Department: Medicina Molecolare e Biotecnologie Mediche
Scuola di dottorato: Scienze biologiche
Dottorato: Biochimica e biologia cellulare e molecolare
Ciclo di dottorato: 26
Coordinatore del Corso di dottorato:
nomeemail
Arcari, Paolopaolo.arcari@unina.it
Tutor:
nomeemail
Russo, GiuliaUNSPECIFIED
Missero, CaterinaUNSPECIFIED
Date: 30 March 2014
Number of Pages: 66
Uncontrolled Keywords: rpL3, extraribosomal function, ribosomal stress, DNA damage, p21
Settori scientifico-disciplinari del MIUR: Area 05 - Scienze biologiche > BIO/10 - Biochimica
Area 05 - Scienze biologiche > BIO/11 - Biologia molecolare
Aree tematiche (7° programma Quadro): SALUTE e TUTELA DEL CONSUMATORE > Biotecnologie, strumenti e tecnologie generiche per la salute umana
Date Deposited: 09 Apr 2014 10:17
Last Modified: 26 Jan 2015 11:45
URI: http://www.fedoa.unina.it/id/eprint/9818

Abstract

It is now largely accepted that ribosomal proteins may be implicated in a variety of biological functions besides that of components of the translation machinery. Many evidences show that a subset of ribosomal proteins are involved in the regulation of the cell cycle and apoptosis through modulation of p53 activity. In addition, p53-independent mechanisms of cell cycle arrest in response to alterations of ribosomal proteins availability have been described. Here, I identify human rpL3 as a new regulator of cell cycle and apoptosis through the regulation of p21 expression in a p53-independent system. In particular, DNA damage induces accumulation of free-ribosome rpL3. This amount of rpL3, regulating p21 expression, is responsible for cell cycle arrest in response to a mild DNA damage, and apoptosis when the damage in higher and not reparable. In addition, the role of rpL3 is partially independent of p21. Taken together, these findings unravel a novel extraribosomal function of rpL3 which acts as ribosomal stress mediator inhibiting cell proliferation or triggering apoptosis in dependence of the nature of the stress.

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