Affinage

ABHD5

1-acylglycerol-3-phosphate O-acyltransferase ABHD5 · UniProt Q8WTS1

Length
349 aa
Mass
39.1 kDa
Annotated
2026-04-28
100 papers in source corpus 39 papers cited in narrative 39 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ABHD5 (CGI-58) is a multifunctional lipid droplet scaffold protein that coordinates triacylglycerol hydrolysis, phospholipid remodeling, epidermal barrier formation, and signaling across adipose, hepatic, cardiac, and immune tissues. ABHD5 lacks intrinsic lipase activity due to an asparagine substitution in its catalytic triad but activates ATGL-mediated triacylglycerol hydrolysis up to 20-fold through direct protein–protein interaction requiring residues R299 and G328; its availability is governed by sequestration on lipid droplets via high-affinity binding to perilipin 1 (C-terminal domain) and PLIN5, which is relieved by PKA-mediated phosphorylation of both perilipin and ABHD5-Ser239 or by direct binding of long-chain acyl-CoA ligands (PMID:16679289, PMID:19850935, PMID:25421061, PMID:26411340, PMID:28211464). Beyond ATGL coactivation, ABHD5 possesses intrinsic lysophosphatidic acid acyltransferase activity, coactivates PNPLA1 for acylceramide biosynthesis essential for the epidermal permeability barrier, acts as a serine protease cleaving HDAC4 to regulate cardiac glucose metabolism, sequesters PNPLA3-I148M on hepatic lipid droplets to promote steatosis, protects BECN1 from CASP3 cleavage to maintain autophagic flux, and retains DPY30 in the cytoplasm to inhibit SET1A-mediated histone methylation (PMID:18606822, PMID:30361410, PMID:31742248, PMID:30802989, PMID:27559856, PMID:34795238). Loss-of-function mutations in ABHD5 cause Chanarin–Dorfman syndrome, characterized by systemic triglyceride accumulation, ichthyosis from defective acylceramide synthesis, and hepatic steatosis (PMID:11590543, PMID:20023287).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 2001 High

    Identifying ABHD5 as the gene mutated in Chanarin–Dorfman syndrome established that this α/β-hydrolase-fold protein with an atypical catalytic triad (Asn replacing Ser) is essential for neutral lipid metabolism in humans.

    Evidence Genetic linkage and mutation screening in CDS families combined with bioinformatic domain analysis

    PMID:11590543

    Open questions at the time
    • No enzymatic or coactivator function yet demonstrated
    • Mechanistic basis of lipid accumulation unknown
  2. 2004 High

    Demonstrating that ABHD5 localizes to lipid droplets via direct binding to perilipin 1's C-terminus and is released upon PKA activation established the regulated-sequestration model for ABHD5 availability.

    Evidence Lipid droplet proteomics, GFP-CGI-58 live imaging, yeast two-hybrid, perilipin mutant analysis in 3T3-L1 adipocytes

    PMID:15136565 PMID:15292255

    Open questions at the time
    • Target enzyme for ABHD5 coactivation not yet identified
    • Mechanism of PKA-mediated release not molecularly defined
  3. 2006 High

    The discovery that ABHD5 directly binds and activates ATGL up to 20-fold—and that CDS mutations abolish this activation—identified the central enzymatic target and mechanistically explained systemic triglyceride accumulation in CDS.

    Evidence In vitro TG hydrolase assay with recombinant proteins, Co-IP, gain/loss-of-function in COS-7 and 3T3-L1 cells, CDS fibroblast rescue

    PMID:16679289

    Open questions at the time
    • Interaction surface between ABHD5 and ATGL undefined
    • ATGL-independent functions not addressed
  4. 2008 High

    Identification of intrinsic LPA acyltransferase activity in purified recombinant ABHD5 revealed that the protein possesses its own catalytic function beyond ATGL coactivation, converting LPA to phosphatidic acid via a conserved HXXXXD motif.

    Evidence Recombinant ABHD5 from E. coli, in vitro acyltransferase assay with substrate specificity, radiolabeled fatty acid incorporation in CDS fibroblasts

    PMID:18606822 PMID:19801371

    Open questions at the time
    • Physiological significance of LPA acyltransferase activity in vivo not established
    • Relationship between acyltransferase and ATGL-coactivation functions unclear
  5. 2009 High

    The CGI-58 knockout mouse revealed two separable functions: systemic TG accumulation (ATGL-dependent) and a lethal skin barrier defect from impaired acylceramide synthesis (ATGL-independent), establishing ABHD5 as a bifunctional protein.

    Evidence Global Cgi-58 knockout mouse with lipid analysis, histology, and skin barrier assays

    PMID:20023287

    Open questions at the time
    • Molecular partner mediating acylceramide synthesis unknown at this stage
    • Relative contributions of ATGL activation vs. acyltransferase activity to each phenotype unclear
  6. 2009 High

    Quantitative live-cell BiFC and FRET resolved the sequential mechanism: PLIN1 sequesters ABHD5 under basal conditions, and PKA phosphorylation of specific perilipin serines (Ser492/Ser517) releases ABHD5 to interact with ATGL on lipid droplets.

    Evidence BiFC and FRET imaging in live cells with perilipin phosphosite mutants, PKA activation

    PMID:19850935

    Open questions at the time
    • Whether ABHD5 itself is phosphorylated during this process was not yet known
    • Stoichiometry of the ABHD5–PLIN1–ATGL complex undefined
  7. 2010 High

    NMR and mutagenesis of the N-terminal tryptophan-rich region (residues 10–31) showed that two amphipathic anchor arms mediate lipid droplet binding, which is prerequisite for ATGL activation—functionally separating LD targeting from catalytic domains.

    Evidence Solution NMR in DPC micelles, tryptophan-to-alanine mutagenesis, subcellular localization and ATGL activation assays

    PMID:20164531 PMID:26350461

    Open questions at the time
    • Full-length ABHD5 structure unavailable
    • How the N-terminal anchor cooperates with perilipin binding unclear
  8. 2014 High

    Identification of PKA phosphorylation at ABHD5-Ser239 showed that ABHD5 itself is directly regulated post-translationally: phosphorylation promotes its dispersion from PLIN1-coated droplets without altering intrinsic ATGL coactivation capacity.

    Evidence Mass spectrometry, phosphomimetic/alanine mutant localization studies, in vitro ATGL coactivation assay

    PMID:25421061

    Open questions at the time
    • Other phosphorylation sites or post-translational modifications not systematically surveyed
    • Kinetic relationship between perilipin and ABHD5 phosphorylation events unresolved
  9. 2014 High

    PLIN1's C-terminal domain was shown to stabilize ABHD5 against proteasomal degradation, explaining why perilipins 2 and 3 cannot fully substitute for PLIN1 in restraining basal lipolysis—and why PLIN1 frameshift mutations cause constitutive lipolysis.

    Evidence BiFC, chimeric perilipin constructs, PLIN1 siRNA, proteasome inhibition assays, PLIN1 frameshift mutation analysis

    PMID:21757733 PMID:24927580

    Open questions at the time
    • Structural basis of PLIN1 C-terminus–ABHD5 interaction unknown
    • Whether ABHD5 degradation differs across tissues not examined
  10. 2015 High

    Discovery that endogenous long-chain acyl-CoAs and synthetic ligands directly bind ABHD5 and release it from perilipins without PKA activation revealed a second, hormone-independent mechanism for controlling lipolysis.

    Evidence Affinity probe labeling of ABHD5, synthetic ligand functional assays in adipocytes and muscle cells, fluorescence complementation

    PMID:26411340

    Open questions at the time
    • Binding site on ABHD5 for acyl-CoA ligands not structurally defined
    • Physiological contexts where ligand-driven (vs. PKA-driven) release dominates remain unclear
  11. 2017 High

    Reciprocal gain- and loss-of-function mutagenesis identified R299 and G328 as the two residues that specifically confer ATGL coactivation, defining a discrete functional surface distinct from LD targeting and perilipin/ligand-binding regions.

    Evidence ABHD4→ABHD5 chimeric mutagenesis in Cos7 cells, brown adipocytes, and artificial lipid droplets with multiple readouts

    PMID:28211464

    Open questions at the time
    • Direct structural visualization of the ABHD5–ATGL interface lacking
    • Whether these residues participate in activation of other PNPLA family members untested
  12. 2018 High

    Demonstrating that ABHD5 recruits PNPLA1 to lipid droplets and stimulates its ω-O-acylceramide biosynthesis—abolished by CDS mutations—identified the molecular mechanism underlying the ATGL-independent skin barrier defect observed in CGI-58 knockout mice.

    Evidence Immunofluorescence, immunoelectron microscopy, cell-based acylceramide production assays, CDS mutant analysis

    PMID:30361410 PMID:30527376

    Open questions at the time
    • Whether ABHD5 allosterically activates PNPLA1 or only promotes its LD recruitment is unresolved
    • Therapeutic rescue of CDS skin phenotype by PNPLA1 modulation not tested
  13. 2019 High

    Discovery that PNPLA3 (especially the I148M steatosis variant) directly binds and sequesters ABHD5 on hepatic lipid droplets—competing with ATGL for ABHD5—mechanistically explained how PNPLA3-I148M promotes hepatic steatosis through ABHD5 titration.

    Evidence Co-IP in liver, in vitro pulldown with purified proteins, liver-specific Cgi-58 KO epistasis, FCCS quantification of binding affinities, domain mapping

    PMID:30802989 PMID:39814233

    Open questions at the time
    • Structural basis of differential PNPLA3 WT vs. I148M affinity for ABHD5 unknown
    • Whether therapeutic ABHD5 ligands can overcome PNPLA3-I148M sequestration untested
  14. 2019 High

    Identification of ABHD5 as a serine protease that cleaves HDAC4 in cardiomyocytes—generating a cardioprotective N-terminal fragment that inhibits MEF2-dependent transcription—revealed an entirely new enzymatic activity independent of lipid metabolism.

    Evidence In vitro and in vivo protease assays, cardiac-specific gene therapy rescue, pressure-overload heart failure model, analysis of failing human hearts

    PMID:31742248

    Open questions at the time
    • Catalytic mechanism and active site for protease activity not structurally characterized
    • Whether other substrates beyond HDAC4 are cleaved unknown
    • Independent replication of protease activity awaited
  15. 2016 Medium

    ABHD5 was shown to protect BECN1 from CASP3-mediated cleavage by directly competing for the cleavage site, maintaining autophagic flux—loss of ABHD5 impairs autophagy and promotes colorectal tumorigenesis independently of ATGL.

    Evidence Co-IP, competition binding assays, autophagic flux assays, ABHD5 KO in CRC cells

    PMID:27559856

    Open questions at the time
    • Structural basis of ABHD5–BECN1 interaction undefined
    • Single-lab finding not yet independently confirmed
    • Whether ABHD5 protease activity contributes to BECN1 protection untested
  16. 2016 High

    Establishing that CGI-58 regulates hepatic TG and DAG levels independently of ATGL (by comparing single vs. double KD mice) showed that ABHD5 has ATGL-independent lipid metabolic functions in liver, possibly through its acyltransferase activity or activation of other PNPLA enzymes.

    Evidence Direct comparison of single vs. double CGI-58/ATGL knockdown mice by ASO, hepatic lipid and inflammation measurements

    PMID:27396333

    Open questions at the time
    • Precise enzyme(s) mediating ATGL-independent hepatic TG hydrolysis not identified
    • Contribution of LPA acyltransferase vs. other activities unclear
  17. 2021 High

    Discovery that ABHD5 binds DPY30 in the cytoplasm and prevents its nuclear translocation—thereby inhibiting SET1A-mediated methylation of YAP and histone H3—linked ABHD5 to epigenetic regulation and cancer stemness control.

    Evidence Co-IP, subcellular fractionation, DPY30 localization imaging, SET1A activity assays, ChIP, CRC cell functional assays

    PMID:34795238

    Open questions at the time
    • Binding interface between ABHD5 and DPY30 not structurally characterized
    • Whether this mechanism operates in normal (non-cancer) tissues unknown
    • Relationship between DPY30 sequestration and ABHD5's lipid droplet functions not explored

Open questions

Synthesis pass · forward-looking unresolved questions
  • A full-length atomic structure of ABHD5 is lacking, leaving the spatial relationships among the N-terminal LD anchor, the ATGL-activating surface (R299/G328), the acyltransferase HXXXXD motif, the ligand-binding pocket, the perilipin-binding region, and the putative protease active site unresolved.
  • No high-resolution structure of full-length ABHD5
  • How a single protein accommodates ATGL coactivation, LPA acyltransferase, and serine protease activities structurally unresolved
  • Comprehensive substrate profiling for the protease activity needed

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0016740 transferase activity 4 GO:0008289 lipid binding 3 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005811 lipid droplet 7 GO:0005829 cytosol 3 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-1430728 Metabolism 12 R-HSA-162582 Signal Transduction 4 R-HSA-168256 Immune System 2 R-HSA-9612973 Autophagy 2 R-HSA-4839726 Chromatin organization 1
Partners
BECN1DPY30HDAC4PLIN1PLIN5PNPLA1PNPLA2PNPLA3

Evidence

Reading pass · 39 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2006 CGI-58/ABHD5 directly interacts with and activates adipose triglyceride lipase (ATGL), stimulating its triacylglycerol hydrolase activity up to 20-fold. CDS-associated point mutations in CGI-58 abolish this ATGL activation. CGI-58/ATGL coexpression attenuates lipid accumulation in COS-7 cells, and antisense RNA-mediated reduction of CGI-58 in 3T3-L1 adipocytes inhibits TG mobilization. In vitro TG hydrolase assay, Co-IP/interaction studies, gain- and loss-of-function cell models, CDS fibroblast rescue experiments Cell metabolism High 16679289
2001 CGI-58 (ABHD5) belongs to the alpha/beta-hydrolase fold family. Its putative catalytic triad contains asparagine instead of the usual serine residue, distinguishing it from classical esterase/lipase/thioesterase subfamily members. Eight distinct loss-of-function mutations in CGI-58 were identified as the genetic cause of Chanarin-Dorfman Syndrome. Genetic linkage, mutation screening, sequence analysis, bioinformatic domain analysis American journal of human genetics High 11590543
2004 CGI-58 localizes to lipid droplet surfaces in differentiated 3T3-L1 adipocytes via a direct interaction with perilipin A (PLIN1). This interaction requires the C-terminal sequence of perilipin A (amino acids 382-429). Activation of cAMP-dependent protein kinase (PKA) by isoproterenol disperses CGI-58 from lipid droplets to the cytoplasm, and this shift is reversible. Proteomic analysis of lipid droplets, CGI-58-GFP live imaging, stable cell lines with perilipin mutants, immunoprecipitation, pharmacological PKA activation/inhibition The Journal of biological chemistry High 15292255
2004 CGI-58 directly interacts with perilipin via yeast two-hybrid and co-localization studies. CDS-associated missense mutations abolish the ability of CGI-58 to be recruited to lipid droplets and weaken binding to perilipin, establishing that loss of this interaction underlies CDS pathogenesis. CGI-58 also interacts with ADRP (perilipin 2). Yeast two-hybrid, GFP-CGI-58 overexpression imaging, CDS mutant analysis in 3T3-L1 and CHO-K1 cells The Journal of biological chemistry High 15136565
2007 CGI-58 knockdown causes abnormal lipid droplet accumulation in 3T3-L1 preadipocytes and Hepa1 hepatoma cells, and reduces both basal and PKA-stimulated lipolysis. CGI-58 itself has no intrinsic lipase/esterase activity but enhances ATGL activity. Upon lipolytic stimulation, CGI-58 disperses from lipid droplets to cytosol, and this depends on perilipin phosphorylation which reduces CGI-58 binding. RNAi knockdown, in vitro lipase activity assay, live-cell imaging, coherent anti-Stokes Raman scattering microscopy Journal of lipid research High 17308334
2009 Perilipin (PLIN1) binds ABHD5 with high affinity, sequestering it and suppressing its interaction with ATGL to reduce basal lipolysis. PKA-mediated phosphorylation of perilipin on Ser492 or Ser517 rapidly releases ABHD5, allowing direct ABHD5–ATGL interaction primarily on lipid droplets containing perilipin. Bimolecular fluorescence complementation (BiFC) in live cells, FRET imaging, protein trafficking experiments, PKA activation studies The Journal of biological chemistry High 19850935
2008 CGI-58 functions as a coenzyme A-dependent lysophosphatidic acid (LPA) acyltransferase, converting LPA to phosphatidic acid. Recombinant CGI-58 purified from E. coli shows acyl-CoA-dependent acyltransferase activity specifically toward LPA but not other lysophospholipids. This activity is associated with a conserved HXXXXD motif in its C-terminus. Recombinant protein expression in E. coli, in vitro acyltransferase assay, S. cerevisiae overexpression, intrinsic tryptophan fluorescence quenching, radiolabeled fatty acid incorporation in CDS fibroblasts The Journal of biological chemistry High 18606822
2009 Recombinant mouse CGI-58 exhibits CoA-dependent acyltransferase activity specifically for lysophosphatidic acid (not other lysophospholipid acceptors), producing phosphatidic acid. It channels fatty acids released from lipolysis into phospholipids in CDS fibroblasts. The enzyme shows preference for arachidonoyl-CoA and oleoyl-CoA and saturation kinetics. Recombinant protein from E. coli, in vitro LPA acyltransferase assay with kinetics, radiolabeled fatty acid tracking in CDS fibroblasts Journal of lipid research High 19801371
2009 CGI-58 knockout mice (Cgi-58−/−) display systemic TG accumulation and severe hepatic steatosis, confirming CGI-58's role in ATGL-mediated TG hydrolysis. Additionally, a lethal skin permeability barrier defect independent of ATGL establishes an ATGL-independent function of CGI-58 in epidermal lipid metabolism, linked to impaired acylceramide synthesis. Global knockout mouse model, lipid analysis, histology, skin barrier assays, lipidomics The Journal of biological chemistry High 20023287
2008 ABHD5 is located in lipid-transporting lamellar granules of differentiating keratinocytes in the granular epidermal layer. CGI-58 knockdown in cultured keratinocytes reduced expression of differentiation markers, establishing a functional role in keratinocyte differentiation and lamellar granule lipid metabolism. Immunoelectron microscopy, anti-CGI-58 antibody immunostaining, siRNA knockdown in human keratinocytes, 3D organotypic cultures The American journal of pathology High 18832586
2008 Mldp (LSDP5/PLIN5) binds ABHD5 and directs it to lipid droplets; this interaction is required for Atgl activation at PLIN5-containing lipid droplets. An ABHD5 mutant (E262K) with greatly reduced Mldp binding cannot prevent lipid droplet accumulation in cells expressing Mldp despite targeting of Atgl. Protein-protein interaction assays in transfected fibroblasts, cardiac muscle fiber microdissection imaging, ABHD5 E262K mutagenesis, lipid droplet morphology assays The Journal of biological chemistry High 19064991
2010 The N-terminal region (amino acids 1–30) of CGI-58 contains a tryptophan-rich stretch that is essential for lipid droplet binding and ATGL activation. N-terminally truncated CGI-58 localizes to cytoplasm and fails to activate ATGL, demonstrating that correct LD localization is required for ATGL-activating function. 3D homology modeling, 1H NMR with DPC micelles, GFP-fusion localization in cultured cells, N-terminal deletion mutagenesis, ATGL activation assays The Journal of biological chemistry High 20164531
2010 G0S2 binds to ATGL independently of CGI-58 and its activity state, and cells co-expressing G0S2 and CGI-58+ATGL cannot stimulate lipid droplet turnover, indicating that CGI-58 and G0S2 regulate ATGL via non-competing mechanisms. Overexpression studies in cells, Co-IP, lipid droplet morphology assays Cell cycle (Georgetown, Tex.) Medium 20676045
2011 The C-terminus of PLIN1 sequesters ABHD5 and inhibits basal ATGL activity. Human frame-shift mutations (Leu404fs, Val398fs) in PLIN1 fail to bind ABHD5 as shown by bimolecular fluorescence complementation, leading to constitutive ABHD5-mediated ATGL coactivation and increased basal lipolysis. siRNA knockdown of ABHD5 or ATGL reversed this increased lipolysis. Bimolecular fluorescence complementation (BiFC), siRNA knockdown of ABHD5/ATGL in stably transfected preadipocytes, lipolysis assays The Journal of biological chemistry High 21757733
2011 The minimal active domain of ATGL (extending to Leu254, beyond the patatin domain to Leu178) can still be activated by CGI-58 and inhibited by G0S2, establishing that the interaction surfaces for both regulators reside within this minimal domain. Domain truncation mutagenesis, in vitro lipase activity assay, protein-protein interaction studies, 3D homology modeling PloS one High 22039468
2014 CGI-58/ABHD5 Ser239 is phosphorylated by protein kinase A (PKA) in vivo. PKA-mediated phosphorylation of CGI-58 at Ser239 is required for its dispersion from perilipin 1A-coated lipid droplets upon lipolytic stimulation, thereby increasing CGI-58 availability for ATGL coactivation. Phosphorylation does not alter ATGL coactivation activity per se. Phosphoamino acid analysis, mass spectrometry, immunoblotting of recombinant and endogenous CGI-58, phosphomimetic/alanine mutant localization studies in cells, in vitro ATGL coactivation assay Journal of lipid research High 25421061
2015 ABHD5 is the direct target of synthetic ligands and endogenous long-chain acyl-CoA ligands that regulate ABHD5–perilipin interactions. Ligand binding to ABHD5 releases it from PLIN1 or PLIN5 without PKA activation, directly activating adipocyte and muscle lipolysis. Affinity probe labeling demonstrated ABHD5 as the direct ligand target. Molecular imaging, affinity probe labeling, synthetic ligand functional assays in adipocytes and muscle cells, fluorescence complementation Cell metabolism High 26411340
2015 NMR structure of the CGI-58 N-terminal tryptophan-rich peptide (residues 10–31) bound to DPC micelles reveals two anchor arms: a left arm (Trp21/Trp25 plus adjacent leucines) and a right arm (Trp29). Simultaneous tryptophan-to-alanine mutations in both arms abolish LD localization and ATGL activation, whereas single-arm mutations do not. Solution-state NMR structure of LD-anchor peptide in DPC micelles, tryptophan-alanine mutagenesis, subcellular localization assays, ATGL activation assays The Journal of biological chemistry High 26350461
2014 Perilipins 2 and 3 lack the C-terminal carboxy-terminal domain of perilipin 1 that binds and stabilizes ABHD5. This C-terminal domain of PLIN1 retards ABHD5 proteasomal degradation. Chimeric PLIN2 or PLIN3 fused with the PLIN1 C-terminus suppress basal lipolysis more effectively by stabilizing ABHD5. Knockdown of PLIN1 in adipocytes reduces ABHD5 expression and LD localization, increasing basal lipolysis. BiFC, chimeric protein construction, PLIN1 siRNA knockdown, ABHD5 protein stability assays (proteasome inhibition) Proceedings of the National Academy of Sciences of the United States of America High 24927580
2017 Two conserved ABHD5 residues (R299 and G328) are specifically required for ATGL lipase activation. Introducing these residues into the ABHD4 paralog (ABHD4 N303R/S332G) conferred ATGL activation ability, and corresponding ABHD5 mutations (R299N, G328S) selectively disrupted lipolysis without affecting ATGL LD translocation or ABHD5 interactions with perilipins/ligands. Structural modeling places these residues on a novel functional surface. Comparative evolutionary analysis, structural modeling, gain-of-function ABHD4 mutagenesis in Cos7 cells/brown adipocytes/artificial lipid droplets, loss-of-function ABHD5 mutagenesis Scientific reports High 28211464
2019 PNPLA3 (wild-type and 148M variant) directly interacts with CGI-58 and requires CGI-58 for its localization to hepatic lipid droplets. PNPLA3 inhibits ATGL activity by competing for CGI-58, and PNPLA3(148M) promotes hepatic steatosis in a CGI-58-dependent manner. Direct PNPLA3–CGI-58 interaction was demonstrated by Co-IP and pulldown with purified proteins. Co-IP in mouse liver, in vitro pulldown with purified proteins, liver-specific Cgi-58 KO mice, HuH-7 cell overexpression, hepatic TG measurement Hepatology (Baltimore, Md.) High 30802989
2019 ABHD5 functions as a serine protease that cleaves HDAC4 in cardiomyocytes, generating an N-terminal HDAC4 polypeptide (HDAC4-NT). This proteolytic activity inhibits MEF2-dependent gene expression and controls glucose handling in the heart. ABHD5 deficiency leads to loss of HDAC4-NT generation and heart failure, independent of lipid accumulation. In vitro and in vivo serine protease assay, cardiac-specific gene therapy (HDAC4-NT), transgenic ABHD5 mouse model, pressure-overload heart failure model, analysis of failing human hearts Nature metabolism High 31742248
2018 ABHD5 directly interacts with PNPLA1 and recruits it to lipid droplets, stimulating PNPLA1-mediated esterification of ω-hydroxy ceramides with linoleic acid to produce ω-O-acylceramide (acylceramide). CDS-associated ABHD5 point mutations fail to stimulate PNPLA1-mediated acylceramide biosynthesis. Acylceramide-producing cell system, immunofluorescence microscopy, ABHD5–PNPLA1 interaction assays, CDS mutant analysis Journal of lipid research High 30361410
2018 ABHD5 enhances PNPLA1-catalyzed acylceramide production by promoting PNPLA1 localization to lipid droplet membranes. Co-expression of ABHD5 with PNPLA1 transforms dispersed PNPLA1 distribution into lipid droplet-associated localization, and ABHD5 CDS mutations reduce this activity. Immunofluorescent microscopy, immunoelectron microscopy, cell-based acylceramide production assay, ABHD5 CDS mutant analysis Journal of dermatological science High 30527376
2016 ABHD5 directly competes with CASP3 for binding to cleavage sites of BECN1 (Beclin 1), thereby preventing BECN1 cleavage by CASP3. ABHD5 deficiency allows CASP3-mediated BECN1 cleavage, impairing autophagic flux and promoting genomic instability and tumorigenesis in colorectal cancer, independent of PNPLA2/ATGL. Co-IP, competition binding assays, autophagic flux assays, ABHD5 KO in CRC cells, clinical tissue correlation Autophagy Medium 27559856
2019 ABHD5 deficiency in macrophages activates mitochondrial ROS production due to impaired PPARγ signaling, which activates the NLRP3 inflammasome, leading to proinflammatory cytokine secretion. Macrophage-specific CGI-58 KO mice show exacerbated HFD-induced insulin resistance and inflammation reversible by anti-ROS treatment or NLRP3 silencing. Macrophage-specific CGI-58 KO mice, anti-ROS treatment, NLRP3 siRNA knockdown, co-culture fat slice assay, mitochondrial function assays Cell reports High 24703845
2014 ABHD5 suppresses spermidine synthase (SRM)-dependent spermidine production in macrophages by inhibiting ROS-dependent expression of C/EBPε, a transcription factor that activates srm gene transcription. Macrophage-specific ABHD5 transgene promotes colorectal cancer growth that is prevented by an additional SRM transgene. In vitro macrophage assays, mouse macrophage-specific transgenic models, SRM transgene rescue experiment, C/EBPε and ROS pathway analysis Nature communications High 27189574
2016 ABHD5 deficiency in macrophages promotes NFκB p65-dependent matrix metalloproteinase (MMP) production independently of its triglyceride metabolic function, as neither triglycerides nor ABHD5-regulated metabolites affected cancer cell migration. Macrophage ABHD5 KO xenograft and genetic cancer models, in vitro migration assays, NFκB pathway analysis, metabolite measurements Cancer research Medium 31439546
2014 Loss of ABHD5 in colon cancer cells induces epithelial-mesenchymal transition by suppressing the AMPKα-p53 pathway, which promotes aerobic glycolysis (Warburg effect). Intestine-specific knockout of Abhd5 in ApcMin/+ mice robustly increases tumorigenesis and malignant transformation. RNAi silencing, intestine-specific KO in ApcMin/+ mice, AMPK/p53 pathway analysis, Warburg effect measurement Cell reports High 25482557
2021 ABHD5 interacts with DPY30 (core subunit of SET1A methyltransferase complex) in the cytoplasm, inhibiting its nuclear translocation and SET1A-mediated methylation of YAP and histone H3. ABHD5 loss allows DPY30 nuclear accumulation, promoting YAP transcriptional activity and c-Met-driven cancer stemness. Co-IP, subcellular fractionation, DPY30 localization imaging, SET1A activity assays, ChIP, CRC cell functional assays Nature communications High 34795238
2012 CGI-58 functions as a lysophosphatidylglycerol acyltransferase, catalyzing reacylation of lysophosphatidylglycerol to phosphatidylglycerol (PG) in an acyl-CoA-dependent manner. Overexpression and knockdown of CGI-58 adversely affect endogenous PG levels in C2C12 cells, and CGI-58 regulates autophagy/mitophagy through effects on cardiolipin synthesis. Recombinant CGI-58 from Sf9 insect cells and mammalian cells, in vitro acyltransferase assay, PG measurement, autophagy/mitophagy assays in C2C12 cells The Journal of biological chemistry Medium 25315780
2020 ABHD5 cooperates specifically with ATGL (not ABHD4) to mobilize lipid droplet triglycerides for hepatitis C virus assembly. ABHD5 residues critical for ATGL activation are required for pro-viral lipolytic function. Grafting these ABHD5 residues onto ABHD4 restored ATGL interaction and pro-viral function; mutating the predicted ABHD5-ATGL interface ablated both lipolysis and HCV assembly support. ABHD4/ABHD5 chimeric mutagenesis, protein interaction assays, lipid droplet lipolysis assays, HCV production assays, ATGL KD/modulation PLoS pathogens High 32542055
2019 Lipid droplet targeting of ABHD5 and PNPLA3 I148M is required for their direct interaction. PNPLA3 I148M has greater association with ABHD5 than WT PNPLA3 (by fluorescence cross-correlation spectroscopy), and the C-terminus of PNPLA3 is sufficient for LD targeting and ABHD5 interaction. PNPLA3 I148M LD targeting is required to promote steatosis in vitro and in liver. Fluorescence cross-correlation spectroscopy (FCCS), molecular modeling, C-terminal domain truncation/chimeric proteins, in vitro steatosis assay, in vivo liver steatosis model The Journal of biological chemistry High 39814233
2020 ABHD5-mediated lipolysis inhibits mTORC1 signaling in prostate cancer cells by elevating intracellular AMP content and activating AMPK. This creates an energy-consuming futile cycle between TG hydrolysis and resynthesis (requiring DGAT1/DGAT2), leading to AMPK activation, mTORC1 inhibition, and cancer cell growth arrest. ABHD5 overexpression and pharmacological lipolysis activation, transcriptomic profiling, AMPK/mTORC1 pathway analysis, DGAT1/2 inhibition, AMP measurement The Journal of biological chemistry Medium 33219129
2016 ABHD5 associates with hepatic lipid droplets and is required for HCV-driven lipid droplet consumption; Chanarin-Dorfman syndrome ABHD5 mutants are mislocalized and unable to support HCV production or LD lipolysis. A novel tribasic motif in ABHD5 determines both lipolytic and pro-viral properties without affecting LD localization. siRNA screen, ABHD5 mutant localization studies, lipid droplet hydrolysis assays, HCV assembly/release assays, tribasic motif mutagenesis PLoS pathogens High 27124600
2013 CGI-58 knockdown sequesters diacylglycerols (DAG) in lipid droplets/ER rather than the plasma membrane, preventing PKCε translocation to the plasma membrane and thereby protecting against DAG-mediated hepatic insulin resistance despite hepatic steatosis. Antisense oligonucleotide KD, hyperinsulinemic-euglycemic clamp, subcellular DAG fractionation, PKCε localization analysis Proceedings of the National Academy of Sciences of the United States of America High 23302688
2019 ATGL/CGI-58 are expressed in intestinal enterocytes and are critical for hydrolysis of a specific lipid droplet pool derived from basolateral (blood) lipid re-uptake, but not for chylomicron synthesis from dietary lipids. Intestine-specific ATGL/CGI-58 double KO mice show massive cLD accumulation independent of dietary lipids. Intestine-specific double KO mouse model, dietary lipid absorption assays, lipid droplet pool characterization Cell reports High 31412256
2016 CGI-58 regulates hepatic TG metabolism and diacylglycerol levels in an ATGL-independent manner; CGI-58 knockdown causes hepatic steatosis in the genetic absence of ATGL. CGI-58 also regulates hepatic inflammation independently of ATGL. Direct comparison of single vs. double CGI-58/ATGL knockdown mice (ASO), hepatic lipid and inflammation measurements Cell reports High 27396333
2010 A murine CGI-58 short splicing isoform (mCGI-58S), lacking exons 2 and 3, localizes to cytoplasm (not LDs), cannot activate ATGL, but retains lysophosphatidic acid acyltransferase activity. This establishes functional dissociation between LD/ATGL activation and LPA acyltransferase activities. cDNA cloning, GFP-fusion localization, ATGL activation assay, LPA acyltransferase assay, LD turnover assay FEBS letters Medium 20083112

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2006 Adipose triglyceride lipase-mediated lipolysis of cellular fat stores is activated by CGI-58 and defective in Chanarin-Dorfman Syndrome. Cell metabolism 738 16679289
2001 Mutations in CGI-58, the gene encoding a new protein of the esterase/lipase/thioesterase subfamily, in Chanarin-Dorfman syndrome. American journal of human genetics 379 11590543
2009 Perilipin controls lipolysis by regulating the interactions of AB-hydrolase containing 5 (Abhd5) and adipose triglyceride lipase (Atgl). The Journal of biological chemistry 312 19850935
2004 Perilipin A mediates the reversible binding of CGI-58 to lipid droplets in 3T3-L1 adipocytes. The Journal of biological chemistry 256 15292255
2009 Neutral lipid storage disease: genetic disorders caused by mutations in adipose triglyceride lipase/PNPLA2 or CGI-58/ABHD5. American journal of physiology. Endocrinology and metabolism 238 19401457
2004 CGI-58 interacts with perilipin and is localized to lipid droplets. Possible involvement of CGI-58 mislocalization in Chanarin-Dorfman syndrome. The Journal of biological chemistry 215 15136565
2019 PNPLA3, CGI-58, and Inhibition of Hepatic Triglyceride Hydrolysis in Mice. Hepatology (Baltimore, Md.) 179 30802989
2009 Growth retardation, impaired triacylglycerol catabolism, hepatic steatosis, and lethal skin barrier defect in mice lacking comparative gene identification-58 (CGI-58). The Journal of biological chemistry 157 20023287
2007 CGI-58 facilitates lipolysis on lipid droplets but is not involved in the vesiculation of lipid droplets caused by hormonal stimulation. Journal of lipid research 136 17308334
2013 CGI-58 knockdown sequesters diacylglycerols in lipid droplets/ER-preventing diacylglycerol-mediated hepatic insulin resistance. Proceedings of the National Academy of Sciences of the United States of America 133 23302688
2010 CGI-58 knockdown in mice causes hepatic steatosis but prevents diet-induced obesity and glucose intolerance. Journal of lipid research 133 20802159
2008 Functional interactions between Mldp (LSDP5) and Abhd5 in the control of intracellular lipid accumulation. The Journal of biological chemistry 122 19064991
2008 CGI-58, the causative gene for Chanarin-Dorfman syndrome, mediates acylation of lysophosphatidic acid. The Journal of biological chemistry 111 18606822
2015 Endogenous and Synthetic ABHD5 Ligands Regulate ABHD5-Perilipin Interactions and Lipolysis in Fat and Muscle. Cell metabolism 101 26411340
2010 Disruption of the Arabidopsis CGI-58 homologue produces Chanarin-Dorfman-like lipid droplet accumulation in plants. Proceedings of the National Academy of Sciences of the United States of America 99 20876112
2010 The N-terminal region of comparative gene identification-58 (CGI-58) is important for lipid droplet binding and activation of adipose triglyceride lipase. The Journal of biological chemistry 98 20164531
2010 Differential control of ATGL-mediated lipid droplet degradation by CGI-58 and G0S2. Cell cycle (Georgetown, Tex.) 95 20676045
2014 Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition. Cell reports 86 25482557
2014 Macrophage CGI-58 deficiency activates ROS-inflammasome pathway to promote insulin resistance in mice. Cell reports 84 24703845
2016 Macrophage ABHD5 promotes colorectal cancer growth by suppressing spermidine production by SRM. Nature communications 82 27189574
2009 CGI-58/ABHD5 is a coenzyme A-dependent lysophosphatidic acid acyltransferase. Journal of lipid research 80 19801371
2011 The minimal domain of adipose triglyceride lipase (ATGL) ranges until leucine 254 and can be activated and inhibited by CGI-58 and G0S2, respectively. PloS one 77 22039468
2013 Skeletal muscle PLIN proteins, ATGL and CGI-58, interactions at rest and following stimulated contraction. American journal of physiology. Regulatory, integrative and comparative physiology 76 23408028
2011 Human frame shift mutations affecting the carboxyl terminus of perilipin increase lipolysis by failing to sequester the adipose triglyceride lipase (ATGL) coactivator AB-hydrolase-containing 5 (ABHD5). The Journal of biological chemistry 76 21757733
2003 Truncation of CGI-58 protein causes malformation of lamellar granules resulting in ichthyosis in Dorfman-Chanarin syndrome. The Journal of investigative dermatology 74 14708602
2013 The α/β hydrolase CGI-58 and peroxisomal transport protein PXA1 coregulate lipid homeostasis and signaling in Arabidopsis. The Plant cell 69 23667126
2014 CGI-58/ABHD5 is phosphorylated on Ser239 by protein kinase A: control of subcellular localization. Journal of lipid research 67 25421061
2008 Chanarin-Dorfman syndrome: deficiency in CGI-58, a lipid droplet-bound coactivator of lipase. Biochimica et biophysica acta 60 19061969
2017 Positive regulation of prostate cancer cell growth by lipid droplet forming and processing enzymes DGAT1 and ABHD5. BMC cancer 58 28877685
2016 ABHD5 interacts with BECN1 to regulate autophagy and tumorigenesis of colon cancer independent of PNPLA2. Autophagy 58 27559856
2014 Perilipins 2 and 3 lack a carboxy-terminal domain present in perilipin 1 involved in sequestering ABHD5 and suppressing basal lipolysis. Proceedings of the National Academy of Sciences of the United States of America 56 24927580
2019 The lipid droplet-associated protein ABHD5 protects the heart through proteolysis of HDAC4. Nature metabolism 55 31742248
2021 ABHD5 inhibits YAP-induced c-Met overexpression and colon cancer cell stemness via suppressing YAP methylation. Nature communications 53 34795238
2019 Macrophage ABHD5 Suppresses NFκB-Dependent Matrix Metalloproteinase Expression and Cancer Metastasis. Cancer research 50 31439546
2007 CGI-58 facilitates the mobilization of cytoplasmic triglyceride for lipoprotein secretion in hepatoma cells. Journal of lipid research 49 17664529
2010 Clinical and genetic characterization of Chanarin-Dorfman syndrome patients: first report of large deletions in the ABHD5 gene. Orphanet journal of rare diseases 48 21122093
2019 Inherited non-alcoholic fatty liver disease and dyslipidemia due to monoallelic ABHD5 mutations. Journal of hepatology 47 30954460
2015 Structure of a CGI-58 motif provides the molecular basis of lipid droplet anchoring. The Journal of biological chemistry 46 26350461
2018 ABHD5 stimulates PNPLA1-mediated ω-O-acylceramide biosynthesis essential for a functional skin permeability barrier. Journal of lipid research 45 30361410
2018 Molecular mechanism of the ichthyosis pathology of Chanarin-Dorfman syndrome: Stimulation of PNPLA1-catalyzed ω-O-acylceramide production by ABHD5. Journal of dermatological science 45 30527376
2012 Regulation of skeletal muscle lipolysis and oxidative metabolism by the co-lipase CGI-58. Journal of lipid research 44 22383684
2017 Molecular Basis of ABHD5 Lipolysis Activation. Scientific reports 42 28211464
2012 CGI-58/ABHD5-derived signaling lipids regulate systemic inflammation and insulin action. Diabetes 42 22228714
2016 Regulation of Hepatic Triacylglycerol Metabolism by CGI-58 Does Not Require ATGL Co-activation. Cell reports 39 27396333
2015 ATGL and CGI-58 are lipid droplet proteins of the hepatic stellate cell line HSC-T6. Journal of lipid research 36 26330055
2020 The ATGL lipase cooperates with ABHD5 to mobilize lipids for hepatitis C virus assembly. PLoS pathogens 35 32542055
2017 Loss of ABHD5 promotes the aggressiveness of prostate cancer cells. Scientific reports 35 29026202
2004 Steatohepatitis and unsuspected micronodular cirrhosis in Dorfman-Chanarin syndrome with documented ABHD5 mutation. The Journal of pediatrics 35 15127008
2014 Comparative gene identification-58 (CGI-58) promotes autophagy as a putative lysophosphatidylglycerol acyltransferase. The Journal of biological chemistry 30 25315780
2010 Crucial role of CGI-58/alpha/beta hydrolase domain-containing protein 5 in lipid metabolism. Biological & pharmaceutical bulletin 30 20190389
2019 ATGL/CGI-58-Dependent Hydrolysis of a Lipid Storage Pool in Murine Enterocytes. Cell reports 29 31412256
2012 Distinct roles for alpha-beta hydrolase domain 5 (ABHD5/CGI-58) and adipose triglyceride lipase (ATGL/PNPLA2) in lipid metabolism and signaling. Adipocyte 29 23145367
2016 ABHD5/CGI-58, the Chanarin-Dorfman Syndrome Protein, Mobilises Lipid Stores for Hepatitis C Virus Production. PLoS pathogens 27 27124600
2014 Deletion of CGI-58 or adipose triglyceride lipase differently affects macrophage function and atherosclerosis. Journal of lipid research 27 25316883
2014 The hepatitis C virus core protein inhibits adipose triglyceride lipase (ATGL)-mediated lipid mobilization and enhances the ATGL interaction with comparative gene identification 58 (CGI-58) and lipid droplets. The Journal of biological chemistry 27 25381252
2009 ABHD5/CGI-58 facilitates the assembly and secretion of apolipoprotein B lipoproteins by McA RH7777 rat hepatoma cells. Biochimica et biophysica acta 27 19211039
2014 Intestinal Cgi-58 deficiency reduces postprandial lipid absorption. PloS one 26 24618586
2020 Western diet induces severe nonalcoholic steatohepatitis, ductular reaction, and hepatic fibrosis in liver CGI-58 knockout mice. Scientific reports 25 32170127
2017 Novel Pharmacological Probes Reveal ABHD5 as a Locus of Lipolysis Control in White and Brown Adipocytes. The Journal of pharmacology and experimental therapeutics 24 28928121
2015 Macrophage CGI-58 deficiency promotes IL-1β transcription by activating the SOCS3-FOXO1 pathway. Clinical science (London, England : 1979) 24 25431838
2008 Severe steatohepatitis in a patient with a rare neutral lipid storage disorder due to ABHD5 mutation. Journal of hepatology 24 18644654
2008 CGI-58 is an alpha/beta-hydrolase within lipid transporting lamellar granules of differentiated keratinocytes. The American journal of pathology 24 18832586
2020 CGI-58: Versatile Regulator of Intracellular Lipid Droplet Homeostasis. Advances in experimental medicine and biology 23 32705602
2020 ABHD5 suppresses cancer cell anabolism through lipolysis-dependent activation of the AMPK/mTORC1 pathway. The Journal of biological chemistry 23 33219129
2022 ABHD5-A Regulator of Lipid Metabolism Essential for Diverse Cellular Functions. Metabolites 22 36355098
2013 Lipid synthesis and processing proteins ABHD5, PGRMC1 and squalene synthase can serve as novel immunohistochemical markers for sebaceous neoplasms and differentiate sebaceous carcinoma from sebaceoma and basal cell carcinoma with clear cell features. Journal of cutaneous pathology 21 23557589
2022 Structural and functional insights into ABHD5, a ligand-regulated lipase co-activator. Scientific reports 20 35173175
2014 Early onset of Chanarin-Dorfman syndrome with severe liver involvement in a patient with a complex rearrangement of ABHD5 promoter. BMC medical genetics 20 24628803
2018 Molecular characterization of ABHD5 gene promoter in intramuscular preadipocytes of Qinchuan cattle: Roles of Evi1 and C/EBPα. Gene 19 30583026
2011 Adipose-selective overexpression of ABHD5/CGI-58 does not increase lipolysis or protect against diet-induced obesity. Journal of lipid research 19 21885429
2010 Molecular analysis of Chanarin-Dorfman syndrome (CDS) patients: Identification of novel mutations in the ABHD5 gene. European journal of medical genetics 19 20307695
2012 Novel nonsense mutation of ABHD5 in Dorfman-Chanarin syndrome with unusual findings: a challenge for genotype-phenotype correlation. European journal of medical genetics 18 22373837
2018 The Expression Pattern of PLIN2 in Differentiated Adipocytes from Qinchuan Cattle Analysis of Its Protein Structure and Interaction with CGI-58. International journal of molecular sciences 17 29723991
2017 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 17 28827091
2020 Downregulated ABHD5 Aggravates Insulin Resistance of Trophoblast Cells During Gestational Diabetes Mellitus. Reproductive sciences (Thousand Oaks, Calif.) 16 32046372
2019 A novel mutation of ABHD5 gene in a Chanarin Dorfman patient with unusual dermatological findings. Lipids in health and disease 16 31883530
2015 Muscle-specific deletion of comparative gene identification-58 (CGI-58) causes muscle steatosis but improves insulin sensitivity in male mice. Endocrinology 16 25751639
2024 Exploring ABHD5 as a Lipid-Related Biomarker in Idiopathic Pulmonary Fibrosis: Integrating Machine Learning, Bioinformatics, and In Vitro Experiments. Inflammation 15 39046603
2020 Circular RNA cMras Suppresses the Progression of Lung Adenocarcinoma Through ABHD5/ATGL Axis Using NF-κB Signaling Pathway. Cancer biotherapy & radiopharmaceuticals 15 32822232
2010 Liver cirrhosis in an infant with Chanarin-Dorfman syndrome caused by a novel splice-site mutation in ABHD5. Acta paediatrica (Oslo, Norway : 1992) 15 20528790
2022 Molecular Modeling of ABHD5 Structure and Ligand Recognition. Frontiers in molecular biosciences 13 35836935
2019 Oncogenic role of ABHD5 in endometrial cancer. Cancer management and research 13 30936746
2006 Fat breakdown: a function for CGI-58 (ABHD5) provides a new piece of the puzzle. Cell metabolism 13 16679288
2013 Acitretin-responsive ichthyosis in Chanarin-Dorfman syndrome with a novel mutation in the ABHD5/CGI-58 gene. Pediatric dermatology 12 23756328
2022 ABHD5 frameshift deletion in Golden Retrievers with ichthyosis. G3 (Bethesda, Md.) 11 34791225
2022 Protective Effects of Tiaoganquzhi Decoction in Treating inflammatory Injury of Nonalcoholic Fatty liver Disease by Promoting CGI-58 and Inhibiting Expression of NLRP3 Inflammasome. Frontiers in pharmacology 11 35586044
2021 Cardiac-specific CGI-58 deficiency activates the ER stress pathway to promote heart failure in mice. Cell death & disease 11 34702801
2012 Alternative splicing and developmental and hormonal regulation of porcine comparative gene identification-58 (CGI-58) mRNA. Journal of animal science 11 22829614
2025 Lipid droplet targeting of the lipase coactivator ABHD5 and the fatty liver disease-causing variant PNPLA3 I148M is required to promote liver steatosis. The Journal of biological chemistry 10 39814233
2019 Thyroid involvement in Chanarin-Dorfman syndrome in adults in the largest series of patients carrying the same founder mutation in ABHD5 gene. Orphanet journal of rare diseases 10 31118107
2016 Macrophage CGI-58 Attenuates Inflammatory Responsiveness via Promotion of PPARγ Signaling. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology 10 26872126
2014 Chanarin-Dorfman syndrome: clinical report and novel mutation in ABHD5 gene. Journal of postgraduate medicine 10 25121381
2010 Identification of a novel splicing isoform of murine CGI-58. FEBS letters 10 20083112
2024 HBB contributes to individualized aconitine-induced cardiotoxicity in mice via interfering with ABHD5/AMPK/HDAC4 axis. Acta pharmacologica Sinica 9 38467717
2022 Knockdown of hepatocyte Perilipin-3 mitigates hepatic steatosis and steatohepatitis caused by hepatocyte CGI-58 deletion in mice. Journal of molecular cell biology 9 36107452
2021 Promotion effect of salt on intramuscular neutral lipid hydrolysis during dry-salting process of porcine (biceps femoris) muscles by inducing phosphorylation of ATGL, HSL and their regulatory proteins of Perilipin1, ABHD5 and G0S2. Food chemistry 9 34815115
2014 CGI-58, a key regulator of lipid homeostasis and signaling in plants, also regulates polyamine metabolism. Plant signaling & behavior 9 24492485
2018 A New Case of Chanarin-Dorfman Syndrome with a Novel Deletion in ABHD5 Gene. Iranian biomedical journal 8 29475365
2022 Improved Stability of Human CGI-58 Induced by Phosphomimetic S237E Mutation. ACS omega 7 35474805
2014 Transgenic CGI-58 expression in macrophages alleviates the atherosclerotic lesion development in ApoE knockout mice. Biochimica et biophysica acta 7 25178844