Nuestros investigadores

Ivan Raimondi 

Publicaciones científicas más recientes (desde 2010)

Autores:  et al.
Revista: HUMAN GENE THERAPY
ISSN 1043-0342  Vol. 30  Nº 11  2019  págs. A2 - A2
Autores: Huarte, Maite, (Autor de correspondencia)
Revista: GENOME BIOLOGY
ISSN 1474-760X  Vol. 18  2017 
A major shift in our understanding of genome regulation has emerged recently. It is now apparent that the majority of cellular transcripts do not code for proteins, and many of them are long noncoding RNAs (lncRNAs). Increasingly, studies suggest that lncRNAs regulate gene expression through diverse mechanisms. We review emerging mechanistic views of lncRNAs in gene regulation in the cell nucleus. We discuss the functional interactions that lncRNAs establish with other molecules as well as the relationship between lncRNA transcription and function. While some of these mechanisms are specific to lncRNAs, others might be shared with other types of genes.
Autores: Huarte, Maite;
Revista: NATURE MEDICINE
ISSN 1078-8956  Vol. 23  Nº 10  2017  págs. 1122 - 1123
Two recent studies show that 'silent' variants can modulate regulatory circuits, including those in noncoding RNAs, affecting cancer predisposition and drug sensitivity.
Autores: Marin-Bejar, O.; Gonzalez, J.; et al.
Revista: GENOME BIOLOGY
ISSN 1474-760X  Vol. 18  2017  págs. 202
BACKGROUND: It is now obvious that the majority of cellular transcripts do not code for proteins, and a significant subset of them are long non-coding RNAs (lncRNAs). Many lncRNAs show aberrant expression in cancer, and some of them have been linked to cell transformation. However, the underlying mechanisms remain poorly understood and it is unknown how the sequences of lncRNA dictate their function. RESULTS: Here we characterize the function of the p53-regulated human lncRNA LINC-PINT in cancer. We find that LINC-PINT is downregulated in multiple types of cancer and acts as a tumor suppressor lncRNA by reducing the invasive phenotype of cancer cells. A cross-species analysis identifies a highly conserved sequence element in LINC-PINT that is essential for its function. This sequence mediates a specific interaction with PRC2, necessary for the LINC-PINT-dependent repression of a pro-invasion signature of genes regulated by the transcription factor EGR1. CONCLUSIONS: Our findings support a conserved functional co-dependence between LINC-PINT and PRC2 and lead us to propose a new mechanism where the lncRNA regulates the availability of free PRC2 at the proximity of co-regulated genomic loci.