Seminar Friday the 10th of November 11.30 am
13 February 2014
The next CRCL/CLB seminar will take place Friday the 10th of November, 11.30am in the ONCORA meeting room (Centre Léon Bérard, 2nd floor). We are pleased to welcome Marat Yusupov (IGBMC, Strasbourg).
2e conference “Stem Cells and Cancer”
13 September 2016
The 2e conference “Stem Cells and Cancer” wwill take place Novembre 15-16, 2016. This event is aimed at bringing together world experts in the fields of embryonic, adult and cancer stem cells. The synergy created by the reunion of leaders at the crossroad of those research themes will highlight novel approaches to address the important challenges associated with stem cells biology and therapeutics.
Information and registration: http://scac.ada.wats-on.co.uk/
Structural Decoding of the Netrin-1/UNC5 Interaction and its Therapeutical Implications in Cancers
25 March 2016
This study involves the team of Patrick Mehlen.
Netrin-1 has been shown to be up-regulated in a fraction of human cancers as a mechanism to allow these tumors to escape the pro-apoptotic activity of some of its main dependence receptors, the UNC5 homologs (UNC5H). Here we identify the V-2 domain of netrin-1 to be important for its interaction with the Ig1/Ig2 domains of UNC5H2. We generate a humanized anti-netrin-1 antibody that disrupts the interaction between netrin-1 and UNC5H2 and triggers death of netrin-1-expressing tumor cells in vitro. We also present evidence that combining the anti-netrin-1 antibody with epidrugs such as decitabine could be effective in treating tumors showing no or modest netrin-1 expression. These results support that this antibody is a promising drug candidate.
PubMed access: click here
Hepatitis B virus X protein identifies the Smc5/6 complex as a host restriction factor
25 March 2016
This study involves Oliver Hantz, in the CRCL team of Isabelle Chemin and Philippe Merle.
Chronic hepatitis B virus infection is a leading cause of cirrhosis and liver cancer. Hepatitis B virus encodes the regulatory HBx protein whose primary role is to promote transcription of the viral genome, which persists as an extrachromosomal DNA circle in infected cells. HBx accomplishes this task by an unusual mechanism, enhancing transcription only from extrachromosomal DNA templates. Here we show that HBx achieves this by hijacking the cellular DDB1-containing E3 ubiquitin ligase to target the 'structural maintenance of chromosomes' (Smc) complex Smc5/6 for degradation. See full abstract on PuMed.