ArticleJournal of lipid research2014
Comparative gene identification 58/α/β hydrolase domain 5 lacks lysophosphatidic acid acyltransferase activity.
Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- A katE katG double-knockout E. coli strain eliminates the risk of catalase contamination in recombinant proteins.Applied microbiology and biotechnology · 2026Article
- CGI-58 Protein Acts as a Positive Regulator of Triacylglycerol Accumulation inJournal of microbiology and biotechnology · 2023Article
- Review
- The genetic interactions between non-alcoholic fatty liver disease and cardiovascular diseases.Frontiers in genetics · 2022Review
- Adipocyte lipolysis: from molecular mechanisms of regulation to disease and therapeutics.The Biochemical journal · 2020Review
- Review
- The α/β-hydrolase domain-containing 4- and 5-related phospholipase Pummelig controls energy storage inJournal of lipid research · 2019Article
- Identification of an intrinsic lysophosphatidic acid acyltransferase activity in the lipolytic inhibitor GFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Adipose Triglyceride Lipase Regulation: An Overview.Current protein & peptide science · 2018Review
- Critical roles for α/β hydrolase domain 5 (ABHD5)/comparative gene identification-58 (CGI-58) at the lipid droplet interface and beyond.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2017Review
- Maternal obesity modulates intracellular lipid turnover in the human term placenta.International journal of obesity (2005) · 2017Article
- Skin Barrier Development Depends on CGI-58 Protein Expression during Late-Stage Keratinocyte Differentiation.The Journal of investigative dermatology · 2017Article
- Regulation of Hepatic Triacylglycerol Metabolism by CGI-58 Does Not Require ATGL Co-activation.Cell reports · 2016Article
- Article
- The Causative Gene in Chanarian Dorfman Syndrome Regulates Lipid Droplet Homeostasis in C. elegans.PLoS genetics · 2015Article
- CGI-58/ABHD5 is phosphorylated on Ser239 by protein kinase A: control of subcellular localization.Journal of lipid research · 2015Article
- Lipid droplet protein LID-1 mediates ATGL-1-dependent lipolysis during fasting in Caenorhabditis elegans.Molecular and cellular biology · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in the gene encoding comparative gene identification 58 (CGI-58)/α/β hydrolase domain 5 (ABHD5) cause Chanarin-Dorfman syndrome, characterized by excessive triacylglycerol storage in cells and tissues. CGI-58 has been identified as a coactivator of adipose TG lipase (ATGL) and a lysophosphatidic acid acyltransferase (LPAAT). We developed a molecular model of CGI-58 structure and then mutated predicted active site residues and performed LPAAT activity assays of recombinant WT and mutated CGI-58. When mutations of predicted catalytic residues failed to reduce LPAAT activity, we determined that LPAAT activity was due to a bacterial contaminant of affinity purification procedures, plsC, the sole LPAAT in Escherichia coli Purification protocols were optimized to reduce plsC contamination, in turn reducing LPAAT activity. When CGI-58 was expressed in SM2-1(DE3) cells that lack plsC, lysates lacked LPAAT activity. Additionally, mouse CGI-58 expressed in bacteria as a glutathione-S-transferase fusion protein and human CGI-58 expressed in yeast lacked LPAAT activity. Previously reported lipid binding activity of CGI-58 was revisited using protein-lipid overlays. Recombinant CGI-58 failed to bind lysophosphatidic acid, but interestingly, bound phosphatidylinositol 3-phosphate [PI(3)P] and phosphatidylinositol 5-phosphate [PI(5)P]. Prebinding CGI-58 with PI(3)P or PI(5)P did not alter its coactivation of ATGL in vitro. In summary, purified recombinant CGI-58 that is functional as an ATGL coactivator lacks LPAAT activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.