Hypomorphic variants of SEL1L-HRD1 ER-associated degradation are associated with neurodevelopmental disorders
Author:
Funder
National Institutes of Health
Fondazione Telethon
National Ataxia Foundation
Publisher
American Society for Clinical Investigation
Subject
General Medicine
Link
https://www.jci.org/articles/view/170054/files/pdf
Reference86 articles.
1. The Mammalian Endoplasmic Reticulum-Associated Degradation System
2. Quality Control in the Endoplasmic Reticulum: Crosstalk between ERAD and UPR pathways
3. New Insights into the Physiological Role of Endoplasmic Reticulum-Associated Degradation
4. The Delicate Balance Between Secreted Protein Folding and Endoplasmic Reticulum-Associated Degradation in Human Physiology
5. ER-associated degradation in health and disease – from substrate to organism
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1. Endoplasmic reticulum associated degradation preserves neurons viability by maintaining endoplasmic reticulum homeostasis;Frontiers in Neuroscience;2024-07-29
2. Purkinje Cell-specific Deficiency in SEL1L-HRD1 Endoplasmic Reticulum-Associated Degradation Causes Progressive Cerebellar Ataxia in Mice;2024-06-26
3. Transcriptomic analysis of SEL1L and HRD1 knockout cell lines reveals multifaceted roles of SEL1L beyond the ER quality control;2024-06-12
4. SEL1L-HRD1 interaction is required to form a functional HRD1 ERAD complex;Nature Communications;2024-02-16
5. Proteomic screens of SEL1L-HRD1 ER-associated degradation substrates reveal its role in glycosylphosphatidylinositol-anchored protein biogenesis;Nature Communications;2024-01-22
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