https://pages.htgaa.org/2026a/flo-razoux/homework/week_05_hw/index.htmlHugoenhttps://pages.htgaa.org/2026a/flo-razoux/homework/week_05_hw/sod1-binder-peptide-design/index.htmlMon, 01 Jan 0001 00:00:00 +0000https://pages.htgaa.org/2026a/flo-razoux/homework/week_05_hw/sod1-binder-peptide-design/index.htmlIntro from Pranam Chatterjee Superoxide dismutase 1 (SOD1) is a cytosolic antioxidant enzyme that converts superoxide radicals into hydrogen peroxide and oxygen. In its native state, it forms a stable homodimer and binds copper and zinc. Mutations in SOD1 cause familial Amyotrophic Lateral Sclerosis (ALS). Among them, the A4V mutation (Alanine → Valine at residue 4) leads to one of the most aggressive forms of the disease. The mutation subtly destabilizes the N-terminus, perturbs folding energetics, and promotes toxic aggregation.https://pages.htgaa.org/2026a/flo-razoux/homework/week_05_hw/brd4-drug-discovery-boltz-lab/index.htmlMon, 01 Jan 0001 00:00:00 +0000https://pages.htgaa.org/2026a/flo-razoux/homework/week_05_hw/brd4-drug-discovery-boltz-lab/index.htmlBOLTZ LAB SKIP FOR NOW ⏱https://pages.htgaa.org/2026a/flo-razoux/homework/week_05_hw/l-protein-mutants-final-project/index.htmlMon, 01 Jan 0001 00:00:00 +0000https://pages.htgaa.org/2026a/flo-razoux/homework/week_05_hw/l-protein-mutants-final-project/index.htmlFinal Group Project TO BE UPDATED on March 31st.