News

Seminars

Seminars

  • Seminar 18th April 2014 - JL Requin meeting room

    21 February 2014
    We are pleased to welcome Dr François Ducray, Neurooncologist at the Hôpital Pierre Wertheimer - Lyon. Please note we will meet in the J-L REQUIN meeting room (CHENEY D), 11.30 am. Title of his talk : "Towards personalized therapy for adult patients with glioma". For more information, click here 

Conferences

Conferences

  • 23rd EACR Congress - Munich 5-8 July 2014

    04 April 2014

    from Basic Research to Personalised Cancer Treatment
    More information and registration: chick here

  • Congress and conference in oncology - EACR

    11 March 2013
    You can find on the EACR website  various congresses, symposiums or workshops in the field of oncology research. More information: click here
Scientific news

Scientific news

  • Endothelial, epithelial, and fibroblast cells exhibit specific splicing programs independently of th

    18 February 2014

    Alternative splicing significantly increases the diversity of transcripts, allowing the human genome to encode from 100.000 to 1.000.000 proteins from only ~22.000 genes. A primitive view of alternative splicing established that different tissues/organs express their own splicing variants, although these tissues are composed of multiple cell types including epithelial, endothelial and fibroblastic cells. Thanks to large scale analyses performed on ENCODE consortium data and after extensive validation by RT -PCR, the CRCL team headed by Didier Auboeuf show that each of these three cell types express its own splicing program independently of its tissue of origin. These programs result from the relative expression and activity of several splicing factors (ESRP1/2, MBNL, PTBP1, NOVA1 and RBFOX2) in the different cell types. All the data are available on FasterDB, a user-friendly web interface that describes the known splicing variants of all human and mouse genes. FasterDB allows to examine the splicing profile of genes through several dozens of tissues and cell lines (normal and cancerous), and to associate this profile to one or more splicing factors, thanks to an integrated visualization interface of CLIP-Seq and exon array data. Thus, each researcher can, through FasterDB, look for the expression profile of his splicing variant of interest in different cell lines/tissues and find the splicing factor(s) that regulate it.
    Access to PubMed:
    click here

  • The dependence receptor TrkC triggers mitochondria dependent apoptosis upon Cobra-1 recruitment

    06 December 2013

    The neurotrophin receptor TrkC was recently identified as a dependence receptor, and, as such, it triggers apoptosis in the absence of its ligand, NT-3. The molecular mechanism for apoptotic engagement involves the double cleavage of the receptor’s intracellular domain, leading to the formation of a proapoptotic ‘‘killer’’ fragment (TrkC KF). The CRCL team headed by P. Mehlen show that TrkC KF interacts with Cobra1, a putative cofactor of BRCA1, and that Cobra1 is required for TrkC-induced apoptosis. This study (Ichim G, Genevois AL, Ménard M, Yu LY, Coelho-Aguiar JM, Llambi F, Jarrosson-Wuilleme L, Lefebvre J, Tulasne D, Dupin E, Le Douarin N, Arumäe U, Tauszig-Delamasure S, Mehlen P,Mol Cell. 2013 Sep 12;51(5):632-46) also show that, in the developing chick neural tube, NT-3 silencing is associated with neuroepithelial cell death that is rescued by Cobra1 silencing. Cobra1 shuttles TrkC KF to the mitochondria, where it promotes Bax activation, cytochrome c release, and apoptosome-dependent apoptosis. Thus, we propose that, in the absence of NT-3, the proteolytic cleavage of TrkC leads to the release of a killer fragment that triggers mitochondria-dependent apoptosis via the recruitment of Cobra1.
    Access to PubMed  :  click here

Job opportunities

Job opportunities

  • Postdoc position

    04 April 2014
    Dr Julien Marie's lab  is looking for a motivated post-doctoral candidate to study the effects of Transforming Growth Factor β on the regulation of T cell immune response. More information: here
Calls

Calls