Investor-State Dispute Settlement (ISDS), Germany and the Transatlantic Relationship

The European Union (EU) has negotiated a comprehensive trade and investment agreement with Canada, and is currently negotiating one with the United States (US). Investor-State Dispute Settlement (ISDS), a provision in most Bilateral Investment Treaties (BITs) and other International Investment Agreements (IIAs), gives investors the right to pursue arbitration with a state. The inclusion of this mechanism in both the Transatlantic Trade and Investment Partnership (TTIP) between the EU and the US, and the Comprehensive Economic and Trade Agreement (CETA) between the EU and Canada has caused considerable public concern. Germany, as one of the most vocal opponents to ISDS in these trade agreements, is making headlines arguing in favor of removing ISDS provisions from the agreements, threatening the continuation of the TTIP negotiations and the ratification of the CETA. Germany has a longstanding history of negotiating BITs containing ISDS. As one of the originators of the concept, it seems surprising for many viewers to see Germany now opposing investment protection. This essay will argue that Germany is seen as opposing the inclusion of ISDS in both the CETA and the TTIP primarily because it does not want it included in the TTIP with the US. Germany’s perceived opposition to ISDS in the CETA is thereby tied to the strategically more important TTIP. This essay is aimed to be part of a larger research effort designed to look at the transatlantic investment protection and ISDS debate. What are the pros and cons of investment protection? Is it a necessary component of transatlantic trade and investment agreements? Could the CETA and the TTIP play a role in setting global, more modern investment protection standards? Examining these possible factors of why the US, Canada and the EU behave the way they do with respect to this debate and casting them against some of the facts of how ISDS works and some of the rulings that have been made with respect to ISDS in the past, future research as part of an PhD hopes to contribute to the larger scholarship on foreign direct investment and the direction thereof. Any suggestions, comments and feedback with respect to either this paper or the intended future research in terms of designing a research proposal for possible PhD applications are welcome

The human G protein β4 subunit: gene structure, expression, Gγ and effector interaction

AbstractThe aim of this study was the characterization of the human Gβ4 subunit of heterotrimeric G proteins. Human Gβ4 is widely expressed. Its gene is located on chromosome 3 with a genomic structure indistinguishable from that of the genes of Gβ1 to Gβ3, but entirely different from Gβ5. In vitro translation co-precipitation analyses revealed that Gβ4 can form stable dimers with Gγ1, Gγ2, Gγ3, Gγ4, Gγ5, Gγ7, Gγ10, Gγ11, Gγ12, and Gγ13, dimers which were also able to stimulate phospholipase β2

Identification and characterization of G beta 3s2, a novel splice variant of the G-protein beta 3 subunit.

The T-allele of a polymorphism (C825T) in the gene for the G-protein beta 3 subunit (GNB3) is associated with cardiovascular and metabolic disorders, distinct cellular features and altered drug responses. The molecular mechanisms that give rise to this complex phenotype have been linked to the occurrence of G beta 3s, a splice variant of GNB3. G beta 3s is predominantly expressed in cells with the 825T-allele. In the present study we describe the identification and characterization of an additional G beta 3 splice variant referred to as G beta 3s2. Its mRNA is expressed in heart, blood cells and tumour tissue, and its expression is also tightly associated with the GNB3 825T-allele. G beta 3s2 is generated by alternative splicing using non-canonical splice sites. G beta subunits belong to the family of propeller proteins and consist of seven regular propeller blades. Transcripts for G beta 3s2 are lacking 129 bp of the coding sequence of the wild-type G beta 3 protein. Thus the predicted structure consists of only six propeller blades, which resembles the structure of G beta 3s. Co-immunoprecipitation analyses indicated that G beta 3s2 dimerizes with different G gamma subunits, e.g. G gamma 5, G gamma 8(C) and G gamma 12. In Sf9 insect cells, expression of G beta 3s2 together with G gamma 12 enhances receptor-stimulated activation of G alpha(i2). Expression of G beta 3s2 in mammalian cells activated the mitogen-activated protein kinase cascade. Together, these results suggest that G beta 3s2 is a biologically active G beta variant which may play a role in the manifestation of the complex phenotype associated with the 825T-allele