ArticleProceedings of the National Academy of Sciences of the United States of America2024
AMBRA1 controls the translation of immune-specific genes in T lymphocytes.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Loss of AMBRA1 activates MAPK and angiogenesis signaling pathways in melanoma cells.FEBS open bio · 2026Article
- Single-cell transcriptomics and mouse model phenotyping for biomarker screen of peripheral blood in Huntington's disease.Scientific reports · 2026Article
- Resident CD49aScience advances · 2026Article
- Molecular and genetic evidence for the role of AMBRA1 in suppressing S-phase entry and tumorigenesis.iScience · 2025Article
- Autophagy in orthodontic tooth movement: advances, challenges, and future perspectives.Molecular medicine (Cambridge, Mass.) · 2025Review
- AMBRA1 controls the translation of immune-specific genes in T lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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Authors and funding
18 authors.
Funding
Abstract
T cell receptor (TCR) engagement causes a global cellular response that entrains signaling pathways, cell cycle regulation, and cell death. The molecular regulation of mRNA translation in these processes is poorly understood. Using a whole-genome CRISPR screen for regulators of CD95 (FAS/APO-1)-mediated T cell death, we identified AMBRA1, a protein previously studied for its roles in autophagy, E3 ubiquitin ligase activity, and cyclin regulation. T cells lacking AMBRA1 resisted FAS-mediated cell death by down-regulating FAS expression at the translational level. We show that AMBRA1 is a vital regulator of ribosome protein biosynthesis and ribosome loading on select mRNAs, whereby it plays a key role in balancing TCR signaling with cell cycle regulation pathways. We also found that AMBRA1 itself is translationally controlled by TCR stimulation via the CD28-PI3K-mTORC1-EIF4F pathway. Together, these findings shed light on the molecular control of translation after T cell activation and implicate AMBRA1 as a translational regulator governing TCR signaling, cell cycle progression, and T cell death.
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