Portfolio item number 1
Short description of portfolio item number 1
Short description of portfolio item number 1
Short description of portfolio item number 2
Master's Thesis, ETH Zurich, 2024
Dysregulation of autophagy, a critical cellular process for degrading and recycling cellular components, is linked to aging and various neurodegenerative diseases. The Unc-51-like kinase complex with three additional proteins, FIP200, ATG101, and ATG13, plays a critical role for autophagy initiation. While FIP200’s CLAW domain is one of the most conserved regions across species, its exact function remains unclear. We identified that upon CLAW domain deletion and charge inversion, ATG13 and FIP200 co- localization is diminished. Subsequent immunoprecipitation analysis coupled with proteomic analysis revealed significant depletion of the ATG12-ATG5-ATG16L1 complex in the CLAW deletion and charge inversion conditions. Our findings demonstrate that in vivo, ATG16L1 interacts with a cluster of positively-charged residues on the surface of the FIP200 CLAW domain. This represents a possible mechanism by which ATG16L1 is recruited to the nascent phagophore. ATG16L1 plays an essential role in membrane LC3 lipidation, a vital process for proper autophagosome expansion, cargo recruitment and membrane closure.
Experimental Neurology, 2024
Spinal cord injury (SCI) presents heterogeneously, complicating recovery prediction. We investigated whether routine serological markers measured within seven days post-injury could predict lower extremity motor scores (LEMS) at 52 weeks. Using feature engineering and eight regression models, we compared marker-based predictions against a baseline model of acute LEMS and age. Serological markers did not improve accuracy; the best model achieved a mean absolute error (MAE) of 6.59, matching baseline. However, stratifying patients by initial LEMS (0 vs. >0) improved MAE by 1.20. Thus, routine serological markers offer limited predictive value, but clinically informed stratification enhances performance.
Clinical and Translational Science, 2025
The All of Us research program provides extensive medical history, drug dosage, and genomic data from a diverse U.S. population, creating an opportunity to uncover new links between genetic variation and medication response. Before pursuing novel discoveries, the dataset’s reliability must be assessed. Here, we test whether established drug–gene interactions can be reproduced using electronic health record data from All of Us. Focusing on the CYP450 enzyme family, which metabolizes roughly 90% of clinical drugs, we examine 61 CYP450-metabolized medications and assess dosage differences across metabolizer phenotypes. We replicate several known interactions involving CYP2D6, CYP2C19, CYP2C9, and CYP3A5, though not all expected associations emerge—likely due to data noise, limited dose adjustment in clinical practice, or phenoconversion. Overall, the results demonstrate that All of Us captures a subset of validated pharmacogenomic effects and has strong potential for future PGx discovery.
Published:
This is a description of your talk, which is a markdown file that can be all markdown-ified like any other post. Yay markdown!
Published:
This is a description of your talk, which is a markdown file that can be all markdown-ified like any other post. Yay markdown!
Undergraduate course, University 1, Department, 2014
This is a description of a teaching experience. You can use markdown like any other post.
Workshop, University 1, Department, 2015
This is a description of a teaching experience. You can use markdown like any other post.