Cells maintain health by recycling damaged components through autophagy. This research identifies proteins that connect the endoplasmic reticulum to the growing autophagic membrane, enabling lipid transfer required for cellular waste removal. Understanding this mechanism helps explain how failures in cellular cleaning contribute to aging and diseases such as Alzheimer’s and Parkinson’s.

This research develops small-molecule treatments for chikungunya virus using a lock-and-key approach targeting viral proteins. A key challenge—molecular orientation (enantiomers)—was addressed with a new synthesis method producing over 95% effective molecules. The optimized compound, BDGR-651, shows promise as a future antiviral treatment for this debilitating disease.

This thesis examines how octopuses respond to climate change at a molecular level, focusing on ocean acidification and RNA editing. Rising temperatures harm octopus reproduction, growth, and survival, while acidification produces mixed effects—some species show stress, yet others demonstrate resilience. Cephalopods overall appear more tolerant of acidification than fish, raising questions about the mechanisms behind this adaptability. Thousands of acidification-responsive edits disproportionately affect C2H2 zinc finger regulators, altering predicted binding targets, including nuclear pore components implicated in stress responses.

This research explores how immune-related cells and molecules, beneficial in wound healing, may become harmful in Parkinson’s disease. Using the fruit fly as a model organism, the study investigates which inflammatory processes contribute to brain damage. Early results suggest that excessive activation worsens degeneration, offering potential targets for future therapies.

This research investigates how a gonorrhea protein is processed in E. coli using cellular signal sequences, which act like "ZIP codes" directing the protein to its proper location. By identifying effective signal sequences, the study informs potential molecular targets for earlier detection and better treatment, aiming to prevent gonorrhea-related infertility and improve women's reproductive health.

This research investigates Large Granular Lymphocyte Leukemia, where protective T cells become cancerous. The project explores how DNA methylation silences normal T-cell function and tests drugs that reverse this process. By removing harmful chemical modifications, the goal is to restore immune cells to their healthy, protective “superhero” role.

Cancer often becomes resistant to treatment due to the protein CDK8, which helps reprogram cancer cells. Traditional inhibitors fail because CDK8 still acts as a structural scaffold. This research develops targeted degraders that use the cell’s recycling system to eliminate CDK8 entirely, preventing resistance and improving future cancer therapies.

This research uses yeast to study conserved molecular machinery that ensures safe chromosome division. Focusing on a key cohesin-regulating protein, the work reveals how DNA is accurately separated during cell division and how failures in this system can lead to chromosomal errors, developmental disorders, and cancer.

This research uses fruit flies to study the STING immune pathway, revealing how cells detect viral infections. By identifying Nemo as a missing connector protein active only during infection, the work clarifies how immune responses are triggered. These insights may guide future therapies that balance antiviral defense while limiting immune damage.

This research investigates how MRSA loses its antibiotic resistance by shedding the SCCmec genetic element. Environmental stressors such as heat and dryness increase this vulnerability, while antibiotics alone reinforce resistance. Understanding these mechanisms could enable new strategies to reverse resistance and improve treatment options for life-threatening MRSA infections.