Sima Alavi L&S Biological Sciences
Kinase Regulation of LSG1-VAP Interaction
Defects in ribosomal biogenesis can lead to cancerous cells via dysfunctional p53 protein (a tumor suppressor). This phenomenon is caused by defective ribosomal biogenesis leading to accumulation of 5S RNP, an intermediate in ribosomal assembly. 5S RNP accumulation in turn represses the p53 repressor, inhibiting its function, and rendering p53 in a state of overexpression. Overexpression of p53 is ultimately associated with higher risk of cancer. Therefore, understanding the pathway of ribosomal assembly can provide insight into causes of defective ribosomal cancer cells as well as allude to targets for drug therapy. My research aims to understand the interaction between the large ribosomal subunit’s shuttling protein, Nmd3, with the release protein LSG1, and how these proteins localize and interact with VAPs at the endoplasmic reticulum. Release of Nmd3 allows for the continuation of ribosomal biogenesis, thus understanding all possible interactions and functions of the LSG1 release factor can provide useful insight to how and where defects may occur that ultimately yield defective ribosomes.