R&D Expenditure and GDP in EU Countries

The changes that have taken place in the global economy in recent years have testified to a transformation of an industrial economy into a knowledge-based economy, using technological and innovative potential. This transformation has highlighted the competitive advantages of countries and regions specializing in the production of high-tech products. Innovativeness is considered to be one of the most important factors determining the rate and quality of economic growth. Consequently, highly developed countries are conducting research to seek new sources of innovativeness and methods for creating innovative potential. The key determinants of the innovativeness of an economy are expenditure on research and development and the results of R&D efforts embodied in the form of innovations. The article aims to check a theory by Norwegian economist Jan Fagerberg that the technological potential of an economy, expressed as a relation of R&D expenditure to GDP or as a number of patents per capita, determines positively the rate of GDP growth. In the article, the authors analyze the influence of R&D expenditure on GDP per capita in EU countries in 1999-2008. Panel model estimation methods are used in the research. The results of the analysis show that R&D expenditure determines GDP per capita in the studied countries, the authors conclude

Pharmacological inhibition of CLK2 activates YAP by promoting alternative splicing of AMOTL2

Yes-associated protein (YAP), the downstream effector of the evolutionarily conserved Hippo pathway, promotes cellular proliferation and coordinates certain regenerative responses in mammals. Small molecule activators of YAP may, therefore, display therapeutic utility in treating disease states involving insufficient proliferative repair. From a high-throughput chemical screen of the comprehensive drug repurposing library ReFRAME, here we report the identification of SM04690, a clinical stage inhibitor of CLK2, as a potent activator of YAP-driven transcriptional activity in cells. CLK2 inhibition promotes alternative splicing of the Hippo pathway protein AMOTL2, producing an exon-skipped gene product that can no longer associate with membrane-bound proteins, resulting in decreased phosphorylation and membrane localization of YAP. This study reveals a novel mechanism by which pharmacological perturbation of alternative splicing inactivates the Hippo pathway and promotes YAP-dependent cellular growth