Mutations that bypass tRNA binding activate the intrinsically defective kinase domain in GCN2
The protein kinase GCN2 is activated in amino acid-starved cells on binding of uncharged tRNA to a histidyl-tRNA synthetase (HisRS)-related domain. We isolated two point mutations in the protein kinase (PK) domain, R794G and F842L, that permit strong kinase activity in the absence of tRNA binding. T...
Wedi'i Gadw mewn:
| Cyhoeddwyd yn: | Genes Dev |
|---|---|
| Prif Awduron: | , , , |
| Fformat: | Artigo |
| Iaith: | Inglês |
| Cyhoeddwyd: |
Cold Spring Harbor Laboratory Press
2002
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| Pynciau: | |
| Mynediad Ar-lein: | https://ncbi.nlm.nih.govhttps://pmc.ncbi.nlm.nih.gov/articles/PMC186288/ https://ncbi.nlm.nih.govhttps://pubmed.ncbi.nlm.nih.gov/12023305/ https://ncbi.nlm.nih.govhttps://doi.org/10.1101/gad.979402 |
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