This comparative analysis explores the state repression experienced by The Black Panther Party, which was active mainly during the late 1960s and early 1970s, and the currently biggest movement for racial equality in the US, the Movement for Black Lives. Using Conflict Theory and Critical Race Theory the research asks two research questions: How has state repression changed from the Black Panther Party to the Movement for Black Lives? and What are possible explanations for this change? This thesis aims to shed light on state repression in relation to movements focused on black rights and equality. The findings of this research are in line with conflict theory, and supportive of racial threat perspective as a theoretical framework. The thesis concludes that state repression of black dissent has changed in multiple aspects, such as police violence, legislative measure, surveillance, and media framing, yet is still prevalent and harmful to social movements.

Past literature on transnational repression underscore the significant gap in examining how the relationship between the origin country and the host country influences instances of transnational repression. To fill this gap, this study is bringing in the neglected role of democratic host states by exploring: Why do certain democratic host states encounter significant incidents of transnational repression on their soil while others do not? This essay demystifies the concept of "relationship" and examines whether states, driven by their self-interest, tend to "overlook" transnational repression. This exploration involves testing the hypothesis: An observed comprehensive relationship between the host and origin countries leads to increased transnational repression as the host country tends to “overlook” these incidents. Through a Structured Focused Comparison, the originating country Russia, and the hosting countries Switzerland and the United Kingdom are compared. The findings do not fully support the hypothesis. However, several intriguing discoveries are found that need further investigation.

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<p> Kaiso is a unique member of the BTB/POZ (Broad complex, Tramtrak, Bric à brac,/Pox virus and zinc finger) zinc finger family of transcription factors with established roles in development and tumourigenesis. Kaiso was originally identified as a novel binding partner of the Armadillo catenin p120^ctn, a cytosolic co-factor and regulator of the cell-cell adhesion molecule and tumor suppressor E-cadherin. In addition to their roles in cell adhesion, the multifunctional Armadillo catenins also regulate gene expression, thus providing at least two mechanisms for their contribution to tumourigenesis. The discovery of a novel interaction between p120^ctn and the transcription factor Kaiso was therefore consistent with gene regulatory roles for Armadillo catenins. Interestingly, Kaiso represses transcription via a sequence-specific DNA binding site (TCCTGCnA) as well as through methylated CpG di-nucleotides, and one role of nuclear p120^ctn is to inhibit Kaiso DNA-binding and transcriptional repression. We recently identified sequence-specific Kaiso binding sites in a subset of Wnt/β-catenin/TCF tumour-associated target genes, and here we present data characterizing cyclin D1 as a putative Kaiso target gene.</p> <p> Kaiso binds the cyclin D1 promoter in vitro and in vivo, and artificial promoter assays revealed that Kaiso overexpression results in the repression of a cyclin D1 promoter luciferase reporter. Since cyclin D1 is highly amplified in ~50% of human breast tumours, and a cancer profiling array demonstrated that Kaiso is misexpressed in ~40% of human breast tumours, we hypothesized that Kaiso represses and regulates cyclin D1 expression to inhibit breast tumourigenesis. In fact, examination of Kaiso expression in human breast cell lines demonstrated that cyclin D1 mRNA levels were upregulated in Kaiso-depleted cells. My studies further revealed that methylation-dependent Kaiso-DNA binding may contribute to Kaiso's transcriptional repression of the cyclin D1 promoter. We also determined that Kaiso inhibits, while p120^ctn activates, β-catenin-mediated activation of the cyclin D1 promoter. These findings further support a role for Kaiso and p120^ctn in breast tumourigenesis via their modulation of the canonical Wnt signaling pathway which is highly implicated in human tumourigenesis. Together these findings support our hypothesis that Kaiso regulates cyclin D1 expression. However, further studies are required to elucidate the mechanism employed by Kaiso to elicit cyclin D1 repression and to examine how this activity may contribute to breast tumourigenesis.</p> / Thesis / Master of Science (MSc)