Adriana Ordóñez

This study shows that both terminal misfolding and polymerisation of Z 1-antitrypsin contribute to liver disease phenotypes, with terminal misfolding driving pro-fibrotic responses and metabolic changes.

This study identifies SLC33A1 as a key regulator of ATF6 activation by ER stress, showing its role in metabolite transport and glycan processing.

The paper uses a CRISPR/Cas9 screen to identify calreticulin as a repressor of ATF6α signaling in the unfolded protein response.