{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["65(11)"],"submitter":["Cansby E"],"pubmed_abstract":["Metabolic dysfunction-associated steatotic liver disease has emerged as a leading global cause of chronic liver disease. Our recent translational investigations have shown that the STE20-type kinases comprising the GCKIII subfamily-MST3, STK25, and MST4-associate with hepatic lipid droplets and regulate ectopic fat storage in the liver; however, the mode of action of these proteins remains to be resolved. By comparing different combinations of the silencing of MST3, STK25, and/or MST4 in immortalized human hepatocytes, we found that their single knockdown results in a similar reduction in hepatocellular lipid content and metabolic stress, without any additive or synergistic effects observed when all three kinases are simultaneously depleted. A genome-wide yeast two-hybrid screen of the hum"],"journal":["Journal of lipid research"],"pagination":["100669"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11602991"],"repository":["biostudies-literature"],"pubmed_title":["GCKIII kinases control hepatocellular lipid homeostasis via shared mode of action."],"pmcid":["PMC11602991"],"pubmed_authors":["Xia Y","Mahlapuu M","Henricsson M","Svensson LT","Asiedu B","Andersson E","Hoy AJ","Saghaleyni R","Bluher M","Caputo M","Cansby E"],"additional_accession":[]},"is_claimable":false,"name":"GCKIII kinases control hepatocellular lipid homeostasis via shared mode of action.","description":"Metabolic dysfunction-associated steatotic liver disease has emerged as a leading global cause of chronic liver disease. Our recent translational investigations have shown that the STE20-type kinases comprising the GCKIII subfamily-MST3, STK25, and MST4-associate with hepatic lipid droplets and regulate ectopic fat storage in the liver; however, the mode of action of these proteins remains to be resolved. By comparing different combinations of the silencing of MST3, STK25, and/or MST4 in immortalized human hepatocytes, we found that their single knockdown results in a similar reduction in hepatocellular lipid content and metabolic stress, without any additive or synergistic effects observed when all three kinases are simultaneously depleted. A genome-wide yeast two-hybrid screen of the hum","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2026-06-02T23:10:13.226Z","creation":"2025-04-04T00:46:24.643Z"},"accession":"S-EPMC11602991","cross_references":{"pubmed":["39395791"],"doi":["10.1016/j.jlr.2024.100669"]}}