Seminar of Dr. Rochette-Egly on friday 21st of March
21 February 2014
A seminar will take place with Dr. Cécile Rochette-Egly (INSERM U964, CNRS UMR7104, Université de Strasbourg) on friday 21st March at 11.30 am in the Oncora meeting room (second floor, CLB). The title of his talk is: "Nuclear retinoic acid receptors phosphorylation: structural impact and role in ES cells differentiation": click 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
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 G1, Genevois AL1, Ménard M1, Yu LY, Coelho-Aguiar JM, Llambi F, Jarrosson-Wuilleme L, Lefebvre J, Tulasne D, Dupin E, Le Douarin N, Arumäe U, Tauszig-Delamasure S 2, Mehlen P 2,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
1. these authors contributed equally to this work
2. these co-séniors authors contributed equally to this work