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Populism and Its Effect on International Business Strategy
No full textThis dissertation investigates the complex relationship between populism and international business strategy, with a particular focus on how populist mobilizations influence firms\u27 location decisions and strategic planning. As populism continues to shape political dynamics globally, it presents significant challenges for businesses operating in or considering entry into markets governed by populist regimes. Utilizing institutional theory, this study examines the distinct political risks associated with populism, including anti-establishment ideology, the weakening of democratic institutions, and a tendency toward short-term, reactive policymaking. The research explores the consequences of these risks for firms, particularly in emerging markets, where populism often exacerbates uncertainty and economic volatility. By analyzing the impact of populism on firms\u27 geographic decisions, this dissertation provides insights into the strategic considerations businesses must weigh when operating under populist governments. Additionally, it discusses populism\u27s role in altering democratic processes and its effects on the political environment, which in turn affects corporate strategy. Empirical evidence is drawn from case studies in regions where populism has had a significant impact, such as Latin America and Eastern Europe. These cases highlight the diverse strategies firms employ to mitigate the risks posed by populist regimes, including adapting business models, engaging with local stakeholders, and reassessing their geographic presence. The findings offer a deeper understanding of how political shifts influence business strategy and provide practical guidance for firms seeking to navigate the challenges of operating in politically unstable environments. This study advances international business (IB) literature on the intersection of politics and international business strategy while offering practical recommendations for business leaders and policymakers. It emphasizes the importance of strategic adaptability and the need for comprehensive risk assessment when making location decisions in regions influenced by populism. The insights derived from this research are critical for companies aiming to maintain competitive advantage and achieve long-term success in a rapidly evolving global landscape
Investigating Mediation of Axonal Khsrp Translation and Implications for Nerve Regeneration
No full textAxons can reach long distances throughout our bodies, providing pathways for sensory and motor signaling. However, their considerable lengths make the system vulnerable to disruption by injury and disease. Although PNS axons have the ability to regenerate, the time required for axons to regrow and reinnervate their targets often causes regeneration to fail in humans. Therefore, it is of critical need to develop strategies to enhance neuronal regeneration capacity. Our lab has shown that the RNA binding protein KHSRP slows axon regeneration, as regeneration is accelerated in mice lacking neuronal KHSRP. KHSRP is upregulated injury via Ca2+ → PERK → eIF2aPS51 pathway, and axonal KHSRP remains elevated out to 28 days after axotomy (Patel et al., 2022). All available evidence indicated that the increase in axonal Ca2+ signaling subsides a few hours after initial injury, so it was not clear how KHSRP could remain elevated in regenerating axons. Thus, we looked for potential modulators of KHSRP synthesis and found that REG3A, a secreted calcium-dependent lectin protein that is upregulated in regenerating axons (Kalinski et al., 2015), decreases axon growth, elevates axonal Ca2+, and increases translation of axonal Khsrp mRNA. My project aimed to identify the source of axonal Ca2+ elevation driven by REG3A. We see that primary mouse dorsal root ganglion (DRG) cultures treated with recombinant REG3A (recREG3A) have decreased axon length, increased branching, and increased axonal KHSRP. Using Ca2+ chelators, we find that recREG3A treatment decreases axon growth by inhibiting release of intracellular Ca2+ stores rather than entry into the axons from extracellular sources. Further, inhibitors of ER receptors that are known to mitigate Ca2+ release from the ER partially attenuate effects of recREG3A on both axon growth and elevation of axonal KHSRP. recREG3A increases eIF2a phosphorylation in axons, and this increase as well as the effects on axon growth are blocked by inhibition of PERK. Together, these findings indicate that REG3A slows axon growth by release of axonal ER Ca2+ stores to activate PERK, phosphorylate eIF2a, and increase translation of axonal Khsrp mRNA