AI Article Synopsis
- RAB40C is crucial for lipid droplet homeostasis, with its unique SOCS domain aiding in LD clustering.
- Deletion of RAB40C leads to an increase in lipid droplet accumulation, especially after prolonged oleic acid exposure.
- DAB2IP, a Ras GTPase activating protein, negatively regulates RAB40C's role in lipid droplet homeostasis, suggesting a complex interaction between these proteins and additional signaling pathways.
Article Abstract
Lipid droplet (LD) homeostasis involves activities of various RAB small GTPases. Recently, we found RAB40C was one of the RAB proteins regulating LD homeostasis. RAB40C contains a unique SOCS domain that is required for clustering of LDs. However, its precise functional role in LD homeostasis and mechanism of regulation remain largely unknown. In this study, we observed over-accumulation of LDs in cells with RAB40C deleted by Crispr-Cas9 editing. RAB40C appeared to reduce LD accumulation after long term incubation of cells with oleic acid (24 hours). Unexpectedly, we found that Ras GTPase activating protein (GAP), DAB2IP, bound to RAB40C mainly via its GAP domain and could serve as RAB40C GAP. Studies involving overexpression of DAB2IP and its GAP defective mutant and siRNA depletion of DAB2IP all confirmed that DAB2IP negatively regulated the effect of RAB40C on LD homeostasis. These results provide a novel perspective on the regulation of RAB40C and implicate various signalling pathways regulated by DAB2IP, which may play a role in LD homeostasis via RAB40C.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5689619 | PMC |
| http://dx.doi.org/10.18632/oncotarget.19960 | DOI Listing |
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