Hanna Kuss

Abstract Whole genome and exome sequencing are reporting on hundreds of thousands of missense mutations. Taking a pan-disease approach, we explored how mutations in the intrinsically disordered regions (IDRs) break or generate protein interactions mediated by short linear motifs.

Abstract Whole genome and exome sequencing are reporting on hundreds of thousands of missense mutations. Taking a pan-disease approach, we explored how mutations in the intrinsically disordered regions (IDRs) break or generate short linear motifs. We created a peptide-phage display library tiling peptides overlapping 12,301 disease-associated mutations from the IDRs of the human proteome. The mutations are linked to diverse diseases including cancer, metabolic diseases and neurological diseases.

SARS-CoV-2: From entry to autophagy? SARS-CoV-2, the virus that causes COVID-19, enters cells through endocytosis upon binding to the cell surface receptor ACE2 and potentially others, including integrins. Using bioinformatics, Mészáros et al. predicted the presence of short amino acid sequences, called short linear motifs (SLiMs), in the cytoplasmic tails of ACE2 and various integrins that may engage the endocytic and autophagic machinery. Using affinity binding assays, Kliche et al.