{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Violante S"],"funding":["NIDDK NIH HHS","National Institute of Diabetes and Digestive and Kidney Diseases","National Institutes of Health"],"pagination":["4355-4364"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6404569"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["33(3)"],"pubmed_abstract":["Peroxisomes are essential organelles for the specialized oxidation of a wide variety of fatty acids, but they are also able to degrade fatty acids that are typically handled by mitochondria. Using a combination of pharmacological inhibition and clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR associated protein 9 genome editing technology to simultaneously manipulate peroxisomal and mitochondrial fatty acid β-oxidation (FAO) in HEK-293 cells, we identified essential players in the metabolic crosstalk between these organelles. Depletion of carnitine palmitoyltransferase (CPT)2 activity through pharmacological inhibition or knockout (KO) uncovered a significant residual peroxisomal oxidation of lauric and palmitic acid, leading to the production of peroxisomal acylca"],"journal":["FASEB journal : official publication of the Federation of American Societies for Experimental Biology"],"pubmed_title":["Peroxisomes can oxidize medium- and long-chain fatty acids through a pathway involving ABCD3 and HSD17B4."],"pmcid":["PMC6404569"],"funding_grant_id":["R01DK113172","R01 DK113172"],"pubmed_authors":["Hagen J","Waterham HR","Argmann CA","Achetib N","Yu C","Houten SM","Vaz FM","Violante S","van Roermund CWT","Chen H","Baes M","Dodatko T"],"additional_accession":[]},"is_claimable":false,"name":"Peroxisomes can oxidize medium- and long-chain fatty acids through a pathway involving ABCD3 and HSD17B4.","description":"Peroxisomes are essential organelles for the specialized oxidation of a wide variety of fatty acids, but they are also able to degrade fatty acids that are typically handled by mitochondria. Using a combination of pharmacological inhibition and clustered regularly interspaced short palindromic repeats (CRISPR)-CRISPR associated protein 9 genome editing technology to simultaneously manipulate peroxisomal and mitochondrial fatty acid β-oxidation (FAO) in HEK-293 cells, we identified essential players in the metabolic crosstalk between these organelles. Depletion of carnitine palmitoyltransferase (CPT)2 activity through pharmacological inhibition or knockout (KO) uncovered a significant residual peroxisomal oxidation of lauric and palmitic acid, leading to the production of peroxisomal acylca","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Mar","modification":"2026-06-04T11:18:16.851Z","creation":"2025-06-01T04:03:38.348Z"},"accession":"S-EPMC6404569","cross_references":{"pubmed":["30540494"],"doi":["10.1096/fj.201801498R","10.1096/fj.201801498r"]}}