SMURF2 IN CANCER

"Molecular mechanisms of tumor suppressor functions of HECT-type E3 ligase Smurf2: roles in chromatin organization, dynamics, gene expression and DNA damage response and repair"

Coordinatore	BAR ILAN UNIVERSITY    more  Organization address address: BAR ILAN UNIVERSITY CAMPUS city: RAMAT GAN postcode: 52900 contact info Titolo: Ms Nome: Estelle Cognome: Waise Email: send email Telefono: +972 3 5317439 Fax: +972 3 6353277
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-2013-CIG
Funding Scheme	MC-CIG
Anno di inizio	2013
Periodo (anno-mese-giorno)	2013-08-01   -   2017-07-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	BAR ILAN UNIVERSITY  Organization address address: BAR ILAN UNIVERSITY CAMPUS city: RAMAT GAN postcode: 52900 contact info Titolo: Ms Nome: Estelle Cognome: Waise Email: send email Telefono: +972 3 5317439 Fax: +972 3 6353277	IL (RAMAT GAN)	coordinator	100˙000.00

Mappa

 Word cloud

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

 Obiettivo del progetto (Objective)

'Cancer is a multifaceted disease in which dysregulated gene expression and other aberrant activities are crucial for neoplastic initiation, progression and tumor cell survival upon the treatment with anticancer modalities. One of the major mechanisms that regulate these processes is protein ubiquitination. This modification can impose diverse effects on gene products–proteins, ranging from proteolysis to modulation of protein structure, localization and function. Central components of ubiquitination are the E3 ubiquitin ligases (E3s). Among the different types of E3s, HECT-type E3 ligases are largely unexplored. Recently, the anticancer roles of these enzymes have become highly relevant as we discovered prominent tumor-suppressor functions of one member of this family – Smurf2 (Blank M et al., Nature Med 2012). However, many gaps still remain in our understanding of Smurf2 biological functions in cancer, and potentially important therapeutic targets are missed. The main objective of our research is to delineate the spectrum of molecular mechanisms operating in the cell under the jurisdiction of Smurf2, focusing primarily on those involved in the regulation of chromatin organization and dynamics, gene expression, DNA damage repair and genomic integrity maintenance. They are all interconnected and often compromised in cancer pathways. Using multidisciplinary approaches spanning these areas, we are determined to shed light on roles that HECT-type E3 ligases in general and Smurf2 in particular play in tumor biology and, more importantly, the sensitivity of cancer cells to DNA damage-inducing therapies. Together with surgery, these comprise current first choice in cancer treatment. We believe that the knowledge generated by this study has the potential to provide novel targets in cancer treatment and the design of new, more efficient, therapeutics to combat this devastating disease.'