Masterarbeit, 2011
117 Seiten, Note: 1,0
This work aims to provide a comprehensive overview of the construction and analysis of v-Myb expressing vectors. The work highlights the importance of v-Myb in cell cycle regulation and transformation.
The first chapter of this work introduces the basics of v-Myb, its role in cell cycle regulation and transformation, and the reasons for its study. It explores the relationship between v-Myb and the cell cycle, and its implications for cell growth and proliferation. The chapter also delves into the connection between v-Myb and transformation, examining its potential to induce cancer. The second chapter focuses on the construction of v-Myb expressing vectors. It outlines the process of cloning the v-myb gene, the different types of vectors for stable, transient, inducible, conditional, and specific cell type expression, and the considerations for each type. The third chapter discusses the analysis of v-Myb expression and function. It covers techniques for transfecting cells with v-Myb expressing vectors, analyzing protein and gene expression, and studying cell growth, proliferation, and transformation. The fourth chapter discusses the implications of the findings and potential future directions for research and development.
The key terms and concepts explored in this work include v-Myb, cell cycle regulation, transformation, vector design, expression analysis, and potential applications in research and medicine.
The v-Myb oncogene encodes a transcription factor that regulates gene expression in hematopoietic cells. It can cause cell transformation and arrest cells in an immature stage, leading to leukemia in birds.
Two specific amino acid substitutions in the transactivation domain of v-Myb AMV disrupt its ability to stimulate certain enhancers, such as in the mim-1 gene, and alter its interaction with other proteins like C/EBPβ.
PRMT4 (protein arginine methyltransferase 4) interacts with the hydrophobic region of v-Myb. Interestingly, point mutations in v-Myb AMV appear to increase its affinity for PRMT4 compared to v-Myb E26.
GRP78va is a cytosolic variant of GRP78 that interacts with v-Myb proteins. Experiments show it has a repressing effect on the transactivation potential of v-Myb E26.
These vectors allow scientists to study protein expression, gene regulation, and cell proliferation in a controlled environment to understand cancer development and potential medical treatments.
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