Page 71 - CIBERER-2015-eng

Most relevant scientific articles
Research Groups
di Vona c, BeZdan d, islam aB, salichs e, lóPeZ-Bigas n, ossoWsKi s, de la luna s. Chromatin-wide profiling of DYRK1A reveals a role as a gene-specific RNA polymer- ase II CTD kinase. Mol Cell. 2015;57(3):506-20.
naJas s, arranZ J, lochhead Pa, ashFord al, oxleY d, delaBar Jm, cooK sJ, BaralloBre mJ, arBonés ml. DYR- K1A-mediated Cyclin D1 Degradation in Neural Stem Cells Contributes to the Neurogenic Cortical Defects in Down Syndrome. EBioMedicine. 2015;2(2):120-34.
BoFill-de ros x, santos m, Vila-casadesús m, Villanue- Va e, andreu n, dierssen m, Fillat c. Genome-wide miR-155 and miR-802 target gene identification in the hip-
Highlights
The group focuses its research on the study of the molecular basis, the physiopathological mecha- nisms and therapeutical approaches of neurodevel- opmental genetic diseases with a special interest on aneuploidies associated to human chromosome 21 (HSA21), and towards the development of therapeu- tic strategies for rare tumours. Recently the group, in collaboration with U737, has initiated a new pro- ject for the development of a gene therapy approach for the glutaric aciduria, based on genome editing.
In 2015, team members have identified a new role for the DYRK1A protein kinase as a regulator of specific transcriptional programs, due to the ability of DYRK1A to phosphorylate the C-terminal end of the RNA polymerase II. Such novel activity enlarges the potential effectors that can be modulated upon changes in the kinase levels, as occurs in trisomies or monosomy conditions. Furthermore, it has been demonstrated that DYRK1A regulates cell division (proliferation vs differentiation) in neuronal progen-
pocampus of Ts65Dn Down syndrome mouse model by miRNA sponges. BMC Genomics. 2015;16:907.
catuara-solarZ s, esPinosa-carrasco J, erB i, lang- ohr K, notredame c, gonZáleZ Jr, dierssen m. Principal Component Analysis of the Effects of Environmental En- richment and (-)-epigallocatechin-3-gallate on Age-Asso- ciated Learning Deficits in a Mouse Model of Down Syn- drome. Front Behav Neurosci. 2015 Dec 11;9:330.
BoFill-de ros x, VillanueVa e, Fillat c. Late-phase miR- NA-controlled oncolytic adenovirus for selective killing of cancer cells. Oncotarget. 2015;6(8):6179-90.
itors during development, throughout a process that involves cyclin D1 phoshorylation by DYRK1A, thus contributing to the defect of excitatorial neurons in the cortex of the Ts65Dn mouse model of Down syn- drome (DS). In this model we have also been able to show an association between the extra dose of miR- NA-155 and miRNA-802 with the deregulation of a set of genes with implications in the DS phenotype. Finally, we have demonstrated the beneficial effects of a combined treatment base on (-)-epigallocate- chin-3-gallate (EGCG) and the environmental enrich- ment for the amelioration of age-related cognitive decline in DS and fragile-X syndrome.
With respect to the development of novel therapies for rare tumors we have developed novel oncolytic adenovirus, and generated two patents.
During this year the group has also contributed to the SEFALER Unit.
Institution: Instituto de Investigaciones Biomédicas August Pi i Sunyer Contact: C/ Roselló 149-153. 28036 Barcelona · Tel.: 93 227 54 00 Ext. 4579
CIBERER I Annual report 2015 I 71