Tyburski, Michael D. (2012) The Resource Curse Reversed? Remittances and Corruption in Mexico. International Studies Quarterly, doi: 0.1111/j.1468‐2478.2012.00721.x 
© 2012 International Studies Association Do remittances increase corruption in recipient states? Previous research suggests that remittances allow governments to maintain policies that create corrupt state–society relations. In contrast, this paper argues that remittances mitigate corruption by increasing government accountability and providing other incentives to reform. Using data from Mexico in 2001–2007, this study shows that corruption trended downward in states receiving larger remittance sums, after controlling for political competition, divided government, and market openness. The results are robust to instrumental variable analysis testing for potential endogeneity between corruption and migration. These findings bring attention to remittances as an exogenous resource for reform‐minded groups and suggest that they may operate as the converse of the resource curse.

Keywords: adenosine receptor, breast cancer, cholera toxin, G protein-coupled receptor, protein isoprenylation, protein kinase A (PKA), Ras-related protein 1 (Rap1), b-adrenergic receptor Abbreviations: Adenosine 2B Receptor (A 2 BR), b-adrenergic receptor (bAR), Bay 60-6583 (Bay), Cholera toxin (Ctx), half time (T 1/2 ), Isoproterenol (Iso), G protein-coupled receptors (GPCR), Phosphate buffered saline (PBS), Protein kinase A (PKA), Propranolol (Prop).A greater understanding of the molecular basis of breast cancer metastasis will lead to identification of novel therapeutic targets and better treatments. Rap1B is a small GTPase that suppresses the metastasis of breast cancer cells by increasing cell-cell adhesion. In breast cancer, a decrease in Rap1B prenylation and subsequent loss of Rap1B at the plasma membrane decreases cell-cell adhesion and increases cell scattering, which promotes the metastatic phenotype. Protein kinase A (PKA) was recently found to phosphorylate Rap1B and inhibit its prenylation. PKA is activated by G protein-coupled receptors (GPCR) that stimulate Ga s . In this study, we investigated whether the general Ga s activator, cholera toxin, and agonists of the b-adrenergic receptor (bAR), which is a Ga s -coupled GPCR, promote Rap1B phosphorylation and inhibit its prenylation. We show here that cholera toxin and bAR activation phosphorylate Rap1B and inhibit its prenylation and membrane localization, reducing cell-cell adhesion and promoting cell scattering. Furthermore, we report that breast cancer cell migration is decreased by the FDA-approved b-blocker, propranolol. Pharmacological targeting of GPCRs, especially those such as the bAR that are regulated by FDA-approved drugs, to increase cell adhesion and decrease cell scattering could provide a promising therapeutic approach to reduce breast cancer metastasis.

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