The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.
eIF4GI links nutrient sensing by mTOR to cell proliferation and inhibition of autophagy
Open accessAbstract
Translation initiation factors have complex functions in cells that are not yet understood. We show that depletion of initiation factor eIF4GI only modestly reduces overall protein synthesis in cells, but phenocopies nutrient starvation or inhibition of protein kinase mTOR, a key nutrient sensor. eIF4GI depletion impairs cell proliferation, bioenergetics, and mitochondrial activity, thereby promoting autophagy. Translation of mRNAs involved in cell growth, proliferation, and bioenergetics were selectively inhibited by reduction of eIF4GI, as was the mRNA encoding Skp2 that inhibits p27, whereas catabolic pathway factors were increased. Depletion or overexpression of other eIF4G family members did not recapitulate these results. The majority of mRNAs that were translationally impaired with eIF4GI depletion were excluded from polyribosomes due to the presence of multiple upstream open reading frames and low mRNA abundance. These results suggest that the high levels of eIF4GI observed in many breast cancers might act to specifically increase proliferation, prevent autophagy, and release tumor cells from control by nutrient sensing.
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Cited by
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Metadata
- Authors
- Ramírez-Valle, F., Braunstein, S., Zavadil, J., Formenti, S. C., & Schneider, R. J.
- Venue
- The Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2008-04-21
- Volume
- 181
- Issue
- 2
- Pages
- 293-307
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W2078434966
- Cited by
- 191
- References
- 8
- FWCI
- 3.85
- Type
- journal article
- Language
- en
- Open access
- green
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- Ramírez-Valle, F., Braunstein, S., Zavadil, J., Formenti, S. C., & Schneider, R. J. (2008). eIF4GI links nutrient sensing by mTOR to cell proliferation and inhibition of autophagy. The Journal of Cell Biology. https://doi.org/10.1083/jcb.200710215
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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