
-   G0/G1 Switch Gene 2 (GOS2) controls adipose triglyceride lipase activity and lipid metabolism in skeletal muscle. Recombinant G0S2 protein inhibits ATGL activity by about 40% in lysates of mouse and human skeletal muscle [PMID: 27408777]. ATGL can be inhibited by the protein G0/G1 switch gene 2 (G0S2), acyl-CoA and synthetic inhibitor Atglistatin (which is effective in murine ATGL only) [PMID: 28925902].
-   CIDEC directly interacts with the repressor protein Erg1, leading to binding of Erg1 to the ATGL/PNPLA2 promotor region, which suppresses its transcription [PMID: 24742676].
-   Adipose triglyceride lipase-mediated lipolysis of cellular fat stores is activated by CGI-58 and defective in Chanarin-Dorfman Syndrome [PMID: 16679289].
-   Fat-specific protein 27 (FSP27) interacts with adipose triglyceride lipase (ATGL) to regulate lipolysis and insulin sensitivity in human adipocytes [PMID: 24627478].
-   Perilipin 5 (Plin5) directly interacts with ATGL and CGI-58, and the protein composition of perilipins at the LD surface regulates lipolytic activity of ATGL [PMID: 21393244].
-   Atglistatin selectively inhibits the activity of mouse ATGL in vitro and in vivo [PMID: 24096302]. Long-chain acyl-CoAs non-competitively inhibit ATGL activity [PMID: 24440819].
