Nascent chains can form co-translational folding intermediates that promote post-translational folding outcomes in a disease-causing protein
Alpha-1-antitrypsin (AAT) deficiency results from misfolding-prone AAT variants. Here the authors show that AAT forms co-translational folding intermediates on the ribosome that persist upon release and determine its folding fate. They show too that the ribosome can also modulate misfolding-prone AA...
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| Main Authors: | , , , , , , , |
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| Format: | article |
| Language: | EN |
| Published: |
Nature Portfolio
2021
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| Subjects: | |
| Online Access: | https://doaj.org/article/30b1313e15054f30a9de5b5032f07b04 |
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| Summary: | Alpha-1-antitrypsin (AAT) deficiency results from misfolding-prone AAT variants. Here the authors show that AAT forms co-translational folding intermediates on the ribosome that persist upon release and determine its folding fate. They show too that the ribosome can also modulate misfolding-prone AAT intermediates during their synthesis. |
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