<?xml version="1.0" encoding="utf-8" standalone="yes"?><rss version="2.0" xmlns:atom="http://www.w3.org/2005/Atom"><channel><title>Week 5 HW: Protein Design Part II :: 2026a-ana-gomez</title><link>https://pages.htgaa.org/2026a/ana-gomez/homework/week-05-hw-protein-design-part-ii/index.html</link><description>Week 5: Protein Design Part II Part A: SOD1 Binder Peptide Design (From Pranam): What I know about SOD1 and its mutation: (Berdyński et al., 2022) Mutations in SOD1 cause familial Amyotrophic Lateral Sclerosis (ALS) ALS is a heterogeneous, severe neurodegenerative disorder, the hallmark of which is an adult-onset loss of upper and lower motor neurons. It leads to a progressive paresis and atrophy of skeletal muscles, resulting in quadriplegia and fatal respiratory failure. The mutation subtly destabilizes the N-terminus, perturbs folding energetics, and promotes toxic aggregation. Challenge of this week: Design short peptides that bind mutant SOD1 &amp; then decide which ones are worth advancing toward therapy.</description><generator>Hugo</generator><language>en</language><atom:link href="https://pages.htgaa.org/2026a/ana-gomez/homework/week-05-hw-protein-design-part-ii/index.xml" rel="self" type="application/rss+xml"/></channel></rss>