Joan-Marc Servitja

TL;DR: It is proposed that pancreatic gene programs might be manipulated to generate beta cells or to enhance the function of existing beta cells, thereby providing a possible treatment of different forms of diabetes.

TL;DR: It is shown that Rac1 activity is strongly elevated in Src-transformed cells and that this small G protein is a critical component of the pathway connecting oncogenic Src with cell transformation.

TL;DR: It is shown that the expression of activated forms of G αq and the stimulation of Gq-coupled receptors or chimeric Gαq molecules that respond to Gi-linked receptors can promote a robust activation of endogenous Rho in HEK-293T cells.

TL;DR: It is shown that, at E13-E18, the embryonic stage during which the major burst of beta-cell neogenesis takes place, pancreatic duct cells express Hnf1beta, the product of the maturity-onset diabetes of the young type 5 (MODY5) gene, which is defined as a precursor cellular stage of the embryonic pancreas and placed in a genetic hierarchy that regulates the generation of pancreatic endocrine cells.

TL;DR: The data show that the pattern of circulating miRNAs is modified by defects in glucose metabolism in a similar manner in mice and humans, which could be used as a new diagnostic tool, as well as to monitor response to intervention.