Somma, Domenico
(2013)
CIKS/DDX3X interaction controls the stability of Zc3h12a mRNA induced by IL-17.
[Tesi di dottorato]
| Item Type: |
Tesi di dottorato
|
| Resource language: |
English |
| Title: |
CIKS/DDX3X interaction controls the stability of Zc3h12a mRNA induced by IL-17 |
| Creators: |
| Creators | Email |
|---|
| Somma, Domenico | domenico.somma@unina.it |
|
| Date: |
2 April 2013 |
| Number of Pages: |
71 |
| Institution: |
Università degli Studi di Napoli Federico II |
| Department: |
Biologia e patologia cellullare e molecolare "L. Califano" |
| Scuola di dottorato: |
Medicina molecolare |
| Dottorato: |
Oncologia ed endocrinologia molecolare |
| Ciclo di dottorato: |
25 |
| Coordinatore del Corso di dottorato: |
| nome | email |
|---|
| Santoro, Massimo | massimo.santoro@unina.it |
|
| Tutor: |
| nome | email |
|---|
| Leonardi, Antonio | leonardi@unina.it |
|
| Date: |
2 April 2013 |
| Number of Pages: |
71 |
| Keywords: |
IL-17 DDX3X CIKS |
| Settori scientifico-disciplinari del MIUR: |
Area 05 - Scienze biologiche > BIO/11 - Biologia molecolare
Area 06 - Scienze mediche > MED/04 - Patologia generale |
| Aree tematiche (7° programma Quadro): |
SALUTE e TUTELA DEL CONSUMATORE > Ottimizzazione per la prestazione delle cure sanitarie per i cittadini in Europa |
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| Date Deposited: |
11 Apr 2013 14:08 |
| Last Modified: |
15 Jul 2014 13:16 |
| URI: |
http://www.fedoa.unina.it/id/eprint/9447 |
Collection description
Interleukin 17 (IL-17) promotes the expression of cytokines and proteins involved in inflammation response via the induction of gene transcription and post-transcriptional stabilization of mRNA.
We show here that IL-17 enhanced the stability of zc3h12a mRNA through the RNA binding protein DDX3X. After receptor triggering DDX3X binds the ubiquitin ligase CIKS trough the helicase domain and stabilize zc3h12a mRNA by directly binding the mRNA. This process involved CIKS (but the E3 ubiquitin ligase function is dispensable) the adaptors TRAF2 and TRAF5, and the kinase IKKε.
Zc3h12a is an endonuclease involved in controlling inflammatory responses by degrading mRNA of some inflammatory protein such as IL-6.
This effect is important to correctly switch-off the IL-17-dependent inflammation.
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