School of Science Division of Life Science 29 Mechanistic Investigation of Mitochondrial Quality Control Supervisor: WANG, Lan / LIFS Student: SINGHOF, Michelle / BCB Course: UROP1100, Spring Mitochondria, often termed the powerhouse of the cell, perform a number of essential tasks including but not limited to metabolism, bioenergetics and signalling. Most mitochondrial proteins are encoded by nucleic DNA and thus need to be transported into the mitochondria. This targeting is not always fully correct, so quality control mechanisms are necessary to prevent the accumulation of mistargeted proteins. ATAD1 (Msp1 in yeast) is one such protein that recognizes and removes mistargeted tail-anchored proteins from the outer mitochondrial membrane and mutations in ATAD1 have been linked to several conditions. This project aims to purify ATAD1 as a hexamer for further structural study of ATAD1. G Protein-coupled Receptors in Cell Signaling Supervisor: WONG, Yung Hou / LIFS Student: LEE, Tung Yeung / BCB Course: UROP3100, Fall UROP4100, Spring G-protein alpha-subunit i (Gαi) is a member of the Gαi/o family responsible for inhibiting the activity of adenylate cyclase (AC), which converts ATP to cAMP, a key second messenger involved in a diverse array of intracellular signalling pathways. Hyperactivation of AC disrupts homeostasis. For example, the aberrant transactivation of oncogenes leads to cancer progression and metastasis (Zhang et al. 2020). Despite the important role of Gαi in downregulating the activity of AC to maintain homeostasis, the residues or domains within Gαi involved in its functional interaction with AC have not been fully elucidated. In this study, we employed the GloSensor™ cAMP Assay in the HEK293 cell line to examine the AC-inhibiting abilities of Gαi1 mutants generated using site-directed mutagenesis. Here, we report that residues 209 and 315-318 within the α4-β6 loop of Gαi1 are involved in decreasing the forskolin-stimulated intracellular cAMP levels. G Proteins and their Regulators in Cancer Biology Supervisor: WONG, Yung Hou / LIFS Student: LO, Vincent / BCB Course: UROP2100, Spring Intracellular Nm23-H1 (Non-metastatic protein 23 H1) is a well-studied metastasis suppressor in many cancer cells, but recent studies have implicated it in causing more severe metastasis in neuroblastoma. Moreover, extracellular Nm23-H1 has been found in human serum and culture medium of some cancer cell lines, exhibiting similar functions and properties to its intracellular form. In this study, we investigated the effect of extracellular Nm23-H1 on the migratory ability of the human astrocytoma cell line 1321N1 and confirmed that it upregulates 1321N1 migratory ability, similar to its intracellular form. Furthermore, we discussed current and future directions of research on extracellular Nm23-H1. We believe that extracellular Nm23-H1 has the potential to become a novel therapeutic target in future cancer therapy.
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