AI Article Synopsis
- The KRAS4B oncogene promotes tumor growth when it associates with the plasma membrane, and its movement to the membrane involves a process called farnesylation.
- Researchers identified a G protein-coupled receptor, GPR31, as crucial for this membrane association and found that it interacts with KRAS4B in a manner dependent on farnesylation.
- Silencing GPR31 misplaces KRAS4B and slows the growth of tumor cells dependent on KRAS, highlighting GPR31's role as a chaperone in the secretion pathway for KRAS4B.
Article Abstract
The product of the oncogene, KRAS4B, promotes tumor growth when associated with the plasma membrane (PM). PM association is mediated, in part, by farnesylation of KRAS4B, but trafficking of nascent KRAS4B to the PM is incompletely understood. We performed a genome-wide screen to identify genes required for KRAS4B membrane association and identified a G protein-coupled receptor, GPR31. GPR31 associated with KRAS4B on cellular membranes in a farnesylation-dependent fashion, and retention of GPR31 on the endoplasmic reticulum inhibited delivery of KRAS4B to the PM. Silencing of GPR31 expression partially mislocalized KRAS4B, slowed the growth of KRAS-dependent tumor cells, and blocked KRAS-stimulated macropinocytosis. Our data suggest that GPR31 acts as a secretory pathway chaperone for KRAS4B.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5551702 | PMC |
| http://dx.doi.org/10.1083/jcb.201609096 | DOI Listing |
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