ArticleProceedings of the American Thoracic Society2010
Mechanisms underlying the cellular clearance of antitrypsin Z: lessons from yeast expression systems.
Article in Proceedings of the American Thoracic Society, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Sirtuin3 promotes the degradation of hepatic Z alpha-1 antitrypsin through lipophagy.Hepatology communications · 2024Article
- Serpin neuropathology in the P497S UBQLN2 mouse model of ALS/FTD.Brain pathology (Zurich, Switzerland) · 2021Article
- TorsinA folding and N-linked glycosylation are sensitive to redox homeostasis.Biochimica et biophysica acta. Molecular cell research · 2021Article
- The Autophagy Pathway: A Critical Route in the Disposal of Alpha 1-Antitrypsin Aggregates That Holds Many Mysteries.International journal of molecular sciences · 2021Review
- Erdj3 Has an Essential Role for Z Variant Alpha-1-Antitrypsin Degradation.Journal of cellular biochemistry · 2017Article
- Early-onset torsion dystonia: a novel high-throughput yeast genetic screen for factors modifying protein levels of torsinAΔE.Disease models & mechanisms · 2017Article
- The requirements of yeast Hsp70 of SSA family for the ubiquitin-dependent degradation of short-lived and abnormal proteins.Biochemical and biophysical research communications · 2016Article
- The BiP molecular chaperone plays multiple roles during the biogenesis of torsinA, an AAA+ ATPase associated with the neurological disease early-onset torsion dystonia.The Journal of biological chemistry · 2014Article
- How early studies on secreted and membrane protein quality control gave rise to the ER associated degradation (ERAD) pathway: the early history of ERAD.Biochimica et biophysica acta · 2013Review
- The endosomal protein-sorting receptor sortilin has a role in trafficking α-1 antitrypsin.Genetics · 2012Article
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Authors and funding
2 authors.
Funding
Abstract
The most frequent cause of α(1)-antitrypsin (here referred to as AT) deficiency is homozygosity for the AT-Z allele, which encodes AT-Z. Such individuals are at increased risk for liver disease due to the accumulation of aggregation-prone AT-Z in the endoplasmic reticulum of hepatocytes. However, the penetrance and severity of liver dysfunction in AT deficiency is variable, indicating that unknown genetic and environmental factors contribute to its occurrence. There is evidence that the rate of AT-Z degradation may be one such contributing factor. Through the use of several AT-Z model systems, it is now becoming appreciated that AT-Z can be degraded through at least two independent pathways. One model system that has contributed significantly to our understanding of the AT-Z disposal pathway is the yeast, Saccharomyces cerevisiae.
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Registered trials
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