The EMBO Journal. BRCA2 promotes R‐loop resolution by DDX5 helicase at DNA breaks to facilitate their repair by homologous recombination.
eLife. TRIM37 prevents formation of centriolar protein assemblies by regulating Centrobin.
Nature Communications. TGFβ promotes widespread enhancer chromatin opening and operates on genomic regulatory domains.
eLife. Polo-like kinase acts as a molecular timer that safeguards the asymmetric fate of spindle microtubule-organizing centers.
eLife. Harmful DNA:RNA hybrids are formed in cis and in a Rad51-independet manner.
Misfolding proteins, molecular chaperones and immune dysregulation in neurodegenerative disease
Protein misfolding diseases, e.g. Parkinson’s, Alzheimer’s and ALS, are incurable neurodegenerative disorders characterized by the aberrant aggregation of specific proteins in the brain or CNS, leading to neuron death. Even the pathogenic mechanisms are still poorly understood, dysregulated immune responses are thought to play a major role. The aim of our research is to elucidate the roles and molecular mechanisms of misfolding proteins and immunofunctional heat-shock proteins in immune dysregulation associated to these disorders.
- 14 May 2021
SeminarioMaría García Parajo – Unraveling the dynamic nano- and meso-scale architecture of the living cell membrane
- 21 May 2021
SeminarioHans-Peter Wollsheid – Cytoskeleton meets Chromatin: the role of Myosin VI in DSB repair
- 28 May 2021
SeminarioPlácido Navas – Pathogenic mechanisms of CoQ deficiency
- 04 June 2021
SeminarioSteven West – A CRISPR view of transcriptional termination