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Publication
Mice lacking lipid droplet-associated hydrolase, a gene linked to human prostate
cancer, have normal cholesterol ester metabolism.
Authors Kory N, Grond S, Kamat SS, Li Z, Krahmer N, Chitraju C, Zhou P, Frohlich F,
Semova I, Ejsing C, Zechner R, Cravatt BF, Farese RV, Walther TC
Submitted By Submitted Externally on 2/1/2017
Status Published
Journal Journal of lipid research
Year 2017
Date Published
Volume : Pages 58 : 226 - 235
PubMed Reference 27836991
Abstract Variations in the gene LDAH (C2ORF43), which encodes lipid droplet-associated
hydrolase (LDAH), are among few loci associated with human prostate cancer.
Homologs of LDAH have been identified as proteins of lipid droplets (LDs). LDs
are cellular organelles that store neutral lipids, such as triacylglycerols and
sterol esters, as precursors for membrane components and as reservoirs of
metabolic energy. LDAH is reported to hydrolyze cholesterol esters and to be
important in macrophage cholesterol ester metabolism. Here, we confirm that LDAH
is localized to LDs in several model systems. We generated a murine model in
which Ldah is disrupted but found no evidence for a major function of LDAH in
cholesterol ester or triacylglycerol metabolism in vivo, nor a role in energy or
glucose metabolism. Our data suggest that LDAH is not a major cholesterol ester
hydrolase, and an alternative metabolic function may be responsible for its
possible effect on development of prostate cancer.




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