AI Article Synopsis
- The protein G0S2 acts as an inhibitor of the enzyme ATGL, which is important for breaking down fats in the body.
- Researchers discovered a specific part of G0S2 that effectively inhibits ATGL in both mice and humans without affecting other related lipases.
- This inhibition by G0S2-derived peptides could be a potential new treatment option for managing metabolic disorders linked to increased fat breakdown.
Article Abstract
The protein G0/G1 switch gene 2 (G0S2) is a small basic protein that functions as an endogenous inhibitor of adipose triglyceride lipase (ATGL), a key enzyme in intracellular lipolysis. In this study, we identified a short sequence covering residues Lys-20 to Ala-52 in G0S2 that is still fully capable of inhibiting mouse and human ATGL. We found that a synthetic peptide corresponding to this region inhibits ATGL in a noncompetitive manner in the nanomolar range. This peptide is highly selective for ATGL and does not inhibit other lipases, including hormone-sensitive lipase, monoacylglycerol lipase, lipoprotein lipase, and patatin domain-containing phospholipases 6 and 7. Because increased lipolysis is linked to the development of metabolic disorders, the inhibition of ATGL by G0S2-derived peptides may represent a novel therapeutic tool to modulate lipolysis.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239610 | PMC |
| http://dx.doi.org/10.1074/jbc.M114.602599 | DOI Listing |
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