Affinage

ABHD5

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

Length
349 aa
Mass
39.1 kDa
Annotated
2026-06-09
100 papers in source corpus 34 papers cited in narrative 34 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

ABHD5 (CGI-58) is an α/β-hydrolase-fold lipid droplet-associated protein that serves as the principal co-activator of adipose triglyceride lipase (ATGL), and more broadly as a hub coordinating lipid catabolism with signaling and gene expression (PMID:16679289, PMID:11590543). Although it carries an esterase/lipase/thioesterase-type catalytic triad, the canonical catalytic serine is replaced by asparagine, and ABHD5 itself lacks intrinsic triacylglycerol lipase activity; instead it stimulates ATGL TG hydrolysis up to 20-fold through direct interaction (PMID:16679289, PMID:11590543, PMID:17308334). ATGL activation depends on a defined functional surface (R299, G328) distinct from its other binding activities, and on N-terminal tryptophan-rich anchoring (Trp21/25 and Trp29) that tethers ABHD5 to the lipid droplet, since cytosolic mislocalization abolishes co-activation (PMID:20164531, PMID:26350461, PMID:28211464). ABHD5 availability is controlled by reversible sequestration on perilipin-coated droplets (PLIN1/2/5): perilipins bind and stabilize ABHD5 while suppressing its access to ATGL, and PKA-mediated phosphorylation of both perilipin and ABHD5-Ser239 releases it for lipase activation (PMID:15292255, PMID:19850935, PMID:25421061, PMID:24927580). Beyond ATGL, ABHD5 possesses acyl-CoA-dependent lysophosphatidic acid and lysophosphatidylglycerol acyltransferase activity (PMID:18606822, PMID:19801371, PMID:25315780), and acts as an ATGL-independent regulator of tissue lipid handling, with knockout mice showing systemic TG accumulation, hepatic steatosis, and a lethal skin barrier defect (PMID:20023287, PMID:27396333). In the epidermis it recruits and co-activates PNPLA1 for acylceramide synthesis essential for barrier formation (PMID:30361410), and it mediates the pro-steatotic effect of PNPLA3(I148M) by directing its lipid droplet localization (PMID:30802989, PMID:39814233). ABHD5 additionally functions as a serine protease cleaving HDAC4 to control MEF2-dependent cardiac gene expression (PMID:31742248), protects BECN1 from caspase-3 cleavage to sustain autophagy (PMID:27559856), and restrains tumor growth through metabolic and transcriptional pathways including AMPK/mTORC1 signaling and inhibition of DPY30/SET1A nuclear function (PMID:34795238, PMID:33219129). Loss-of-function mutations in ABHD5 cause Chanarin-Dorfman syndrome, a neutral lipid storage disease with ichthyosis (PMID:11590543).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 2001 High

    Established the gene-disease link and structural identity, defining ABHD5 as an α/β-hydrolase-fold protein with an atypical catalytic triad lacking the canonical serine.

    Evidence Positional cloning and mutation screening in Chanarin-Dorfman syndrome patients with sequence/domain analysis

    PMID:11590543

    Open questions at the time
    • Did not define the molecular function downstream of the mutations
    • Catalytic capacity of the atypical triad left unresolved
  2. 2004 High

    Showed that ABHD5 is recruited to lipid droplets through perilipin binding and is reversibly released to the cytoplasm upon PKA stimulation, placing it in lipolytic signaling.

    Evidence Proteomics, GFP imaging, perilipin deletion mutants, co-IP and isoproterenol/PKA stimulation in adipocytes; yeast two-hybrid with PLIN1/ADRP

    PMID:15136565 PMID:15292255

    Open questions at the time
    • Functional consequence of recruitment for lipase activity not yet defined
    • Y2H/GFP interactions not all confirmed by reciprocal mammalian Co-IP
  3. 2006 High

    Identified the core molecular function: ABHD5 directly binds and activates ATGL to drive TG hydrolysis, with CDS mutants failing to activate, explaining the lipid storage phenotype.

    Evidence Co-expression, in vitro TG hydrolase assays, antisense knockdown, CDS fibroblast complementation, point mutagenesis across multiple cell systems

    PMID:16679289

    Open questions at the time
    • ATGL-binding residues on ABHD5 not yet mapped
    • Did not address non-ATGL functions
  4. 2007 High

    Demonstrated ABHD5 itself lacks lipase/esterase activity and acts purely as a coactivator whose release from droplets depends on perilipin phosphorylation.

    Evidence siRNA knockdown, in vitro lipase assays, live-cell imaging of redistribution in preadipocytes and hepatoma cells

    PMID:17308334

    Open questions at the time
    • Mechanism by which dispersion enables ATGL activation incomplete
    • ABHD5 phosphorylation not yet characterized
  5. 2008 High

    Revealed an intrinsic enzymatic activity distinct from ATGL coactivation: acyl-CoA-dependent LPA acyltransferase generating phosphatidic acid.

    Evidence Recombinant protein from E. coli, in vitro acyltransferase assays, yeast overexpression, adipose tissue MS

    PMID:18606822 PMID:19801371

    Open questions at the time
    • Physiological significance of acyltransferase activity in vivo unresolved
    • Relationship between acyltransferase and coactivator roles unclear
  6. 2008 High

    Extended the perilipin-recruitment model to cardiac muscle and showed PLIN5/Mldp binding is required for ATGL activation at those droplets, generalizing the regulatory mechanism across tissues.

    Evidence In situ Co-IP, co-localization in cardiac fibers and fibroblasts, ABHD5 E262K loss-of-function mutant, lipid droplet assays; lamellar granule localization in keratinocytes

    PMID:18832586 PMID:19064991

    Open questions at the time
    • Skin/keratinocyte function not yet mechanistically tied to a specific enzyme partner
    • Tissue-specific perilipin combinatorics incomplete
  7. 2009 High

    Defined perilipin as a sequestering reservoir whose PKA phosphorylation releases ABHD5 to engage ATGL, establishing the phosphorylation-gated lipolytic switch.

    Evidence FRET/BiFC live-cell imaging and phosphorylation-site mutagenesis in 3T3-L1 adipocytes; constitutive KO mouse showing systemic steatosis and lethal skin defect

    PMID:19850935 PMID:20023287

    Open questions at the time
    • ABHD5 phosphorylation contribution not yet separated from perilipin phosphorylation
    • ATGL-independent skin function molecularly undefined
  8. 2010 High

    Mapped the lipid droplet anchor to an N-terminal tryptophan-rich region and showed correct localization is obligatory for ATGL activation, linking targeting to function.

    Evidence NMR with DPC micelles, GFP localization, deletion mutants, ATGL activation assays; characterization of a cytosolic splice isoform retaining only acyltransferase activity

    PMID:20083112 PMID:20164531

    Open questions at the time
    • Precise anchor residues not yet resolved at structural level (addressed later)
    • Mechanistic basis for acyltransferase retention in cytosolic isoform unclear
  9. 2011 High

    Placed ABHD5 epistatically between PLIN1 and ATGL and localized the coactivation interface to ATGL's minimal patatin-domain fragment, with G0S2 acting as a CGI-58-independent inhibitor.

    Evidence BiFC, siRNA epistasis with human PLIN1 frameshift mutants, ATGL domain truncation, in vitro hydrolase assays and co-IP

    PMID:21757733 PMID:22039468

    Open questions at the time
    • ABHD5 residues contacting ATGL not yet identified
    • Structural model of the ternary regulation absent
  10. 2013 High

    Demonstrated an ATGL-independent metabolic consequence: ABHD5 knockdown sequesters diacylglycerols away from the plasma membrane, preventing PKCε activation and dissociating hepatic DAG from insulin resistance.

    Evidence Antisense knockdown in mice, hyperinsulinemic-euglycemic clamp, subcellular DAG fractionation, PKCε translocation assay

    PMID:23302688

    Open questions at the time
    • Direct molecular target mediating DAG compartmentalization not identified
    • Generalizability beyond liver untested
  11. 2014 High

    Refined the regulatory layer by identifying PKA phosphorylation of ABHD5-Ser239 as the determinant of its release, with perilipin C-terminus also stabilizing ABHD5 against proteasomal degradation.

    Evidence Phosphoamino acid analysis, MS, S239A mutagenesis, localization and in vitro coactivation assays; BiFC, chimeric perilipins and proteasome inhibition

    PMID:24927580 PMID:25421061

    Open questions at the time
    • Whether phosphorylation alters intrinsic coactivation activity ruled out, but downstream conformational effects untested
    • Differential perilipin behavior in non-adipose tissue incompletely mapped
  12. 2014 High

    Broadened the enzymatic and signaling repertoire: ABHD5 reacylates lysophosphatidylglycerol to influence cardiolipin and mitophagy, and macrophage ABHD5 governs PPARγ/ROS/NLRP3 inflammatory signaling.

    Evidence Recombinant Sf9 protein with substrate panel and C2C12 manipulation; macrophage-specific KO mice with NLRP3 silencing and anti-ROS rescue

    PMID:24703845 PMID:25315780

    Open questions at the time
    • Direct link between acyltransferase activity and mitophagy not fully reconstituted
    • Immune phenotype mechanism partly correlative
  13. 2015 High

    Established ABHD5 as a small-molecule and acyl-CoA-responsive switch and resolved the N-terminal anchor structure, showing two independent tryptophan arms are required for droplet binding and ATGL activation.

    Evidence Synthetic ligand screen with affinity probe labeling and FRET/BiFC lipolysis assays; NMR solution structure of the N-terminal peptide with Trp-to-Ala mutagenesis

    PMID:26350461 PMID:26411340

    Open questions at the time
    • Endogenous ligand identity beyond acyl-CoA incomplete
    • Full-length ABHD5 structure still lacking
  14. 2016 High

    Defined a discrete ATGL-activating surface (R299, G328) separable from PLIN/ligand binding and droplet targeting, achieving precise functional dissection of the coactivator role; concurrently revealed ATGL-independent hepatic and autophagy/cancer functions.

    Evidence Gain-of-function transfer to ABHD4 and loss-of-function ABHD5 mutagenesis across cell systems; double-KO mouse hepatic comparison; BECN1/CASP3 competition and autophagy assays; macrophage SRM/spermidine CRC rescue

    PMID:27189574 PMID:27396333 PMID:27559856 PMID:28211464

    Open questions at the time
    • Mechanism coupling lipid metabolism to autophagy and tumor suppression incompletely integrated
    • BECN1 protection shown by single-lab Co-IP/competition assay
  15. 2018 High

    Explained the skin barrier function by showing ABHD5 recruits and co-activates PNPLA1 for acylceramide synthesis, with CDS mutants defective in this activity.

    Evidence Co-expression acylceramide assays, immunofluorescence/immunoelectron microscopy, CDS mutant analysis in HeLa cells

    PMID:30361410 PMID:30527376

    Open questions at the time
    • Whether ABHD5 enzymatic activity contributes to PNPLA1 stimulation unclear
    • Structural basis of ABHD5-PNPLA1 interaction unknown
  16. 2019 High

    Identified two non-lipolytic functions: ABHD5 acts as a serine protease cleaving HDAC4 to control MEF2-dependent cardiac gene expression, and is required for the pro-steatotic localization of PNPLA3(I148M).

    Evidence In vitro proteolysis, in vivo cardiac gene therapy and MEF2 reporter assays; reciprocal Co-IP, purified-protein pulldown and liver-specific Cgi-58 KO epistasis

    PMID:30802989 PMID:31742248

    Open questions at the time
    • How an asparagine-substituted triad supports protease activity unresolved
    • PNPLA3 interaction surface on ABHD5 not mapped at the time
  17. 2020 High

    Extended ATGL coactivation to host-pathogen and growth control: ABHD5-ATGL lipolysis supports HCV particle production, and ABHD5-driven lipolysis activates AMPK/mTORC1 to suppress cancer cell growth.

    Evidence ABHD4/ABHD5 bidirectional mutagenesis with HCV production and lipolysis assays; AMP/ATP and AMPK/mTORC1 signaling with DGAT inhibition in prostate cancer cells

    PMID:32542055 PMID:33219129

    Open questions at the time
    • Generalizability of the futile-cycle growth suppression beyond tested lines unclear
    • Link between viral assembly and specific lipid species incomplete
  18. 2021 High

    Revealed a cytoplasmic transcriptional brake: ABHD5 sequesters DPY30 to block SET1A nuclear function, restraining YAP methylation and c-Met-driven tumor stemness.

    Evidence Co-IP, nuclear fractionation, methyltransferase and YAP methylation assays in CRC cells and mouse models

    PMID:34795238

    Open questions at the time
    • Structural basis of ABHD5-DPY30 interaction unknown
    • Integration with metabolic functions of ABHD5 unclear
  19. 2025 Medium

    Refined the PNPLA3(I148M) mechanism by showing lipid droplet targeting of ABHD5 is required for preferential interaction with the variant and for its steatotic effect.

    Evidence Fluorescence cross-correlation spectroscopy, molecular modeling, C-terminal truncation, in vitro and in vivo steatosis assays

    PMID:39814233

    Open questions at the time
    • Single-lab biophysical study
    • Whether the interaction sequesters ABHD5 from ATGL not directly tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how a single α/β-hydrolase scaffold with an atypical, serine-lacking triad mechanistically supports acyltransferase, HDAC4 protease, and lipase-coactivator activities, and how these are coordinated within and between cell types.
  • No full-length structure resolving the multiple functional surfaces
  • Catalytic mechanism of the reported protease and acyltransferase activities not reconciled with the atypical triad
  • Tissue-specific selection among competing functions undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 3 GO:0060090 molecular adaptor activity 3 GO:0098772 molecular function regulator activity 3 GO:0008289 lipid binding 2 GO:0140096 catalytic activity, acting on a protein 1
Localization
GO:0005811 lipid droplet 4 GO:0005829 cytosol 4 GO:0031410 cytoplasmic vesicle 1
Pathway
R-HSA-1430728 Metabolism 4 R-HSA-162582 Signal Transduction 3 R-HSA-1643685 Disease 3 R-HSA-74160 Gene expression (Transcription) 2 R-HSA-9612973 Autophagy 2
Partners
BECN1DPY30PLIN1PLIN2PLIN5PNPLA1PNPLA2PNPLA3

Evidence

Reading pass · 34 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 TG hydrolase activity up to 20-fold. CDS-associated CGI-58 point mutations fail to activate ATGL. CGI-58/ATGL co-expression attenuates lipid accumulation in COS-7 cells, and antisense-mediated CGI-58 knockdown in 3T3-L1 adipocytes inhibits TG mobilization. Expression of functional CGI-58 in CDS fibroblasts restores lipolysis. Co-expression in COS-7 cells, in vitro TG hydrolase activity assays, antisense RNA knockdown in 3T3-L1 adipocytes, complementation in CDS patient fibroblasts, point-mutation analysis Cell metabolism High 16679289
2001 Mutations in CGI-58 (ABHD5) cause Chanarin-Dorfman syndrome; the CGI-58 protein belongs to the alpha/beta-hydrolase fold family and contains a catalytic triad of the esterase/lipase/thioesterase subfamily, but with asparagine replacing the usual catalytic serine, indicating an atypical or absent classical hydrolase activity. Positional cloning, mutation screening in CDS patients, sequence analysis of protein domain structure American journal of human genetics High 11590543
2004 CGI-58 localizes to lipid droplet surfaces in differentiated 3T3-L1 adipocytes via interaction with perilipin A. The C-terminal sequence (aa 382-429) of perilipin A is required for CGI-58 binding. PKA activation by isoproterenol disperses CGI-58 from lipid droplets to the cytoplasm in a reversible manner. CDS-associated CGI-58 mutants fail to localize to lipid droplets. Proteomics identification, CGI-58-GFP localization in adipocytes, perilipin deletion mutants, immunoprecipitation, isoproterenol/PKA stimulation The Journal of biological chemistry High 15292255
2004 CGI-58 directly interacts with perilipin in a yeast two-hybrid assay and co-localizes to lipid droplet surfaces. CDS-associated CGI-58 mutations (amino acid substitutions) abolish perilipin binding and lipid droplet recruitment. CGI-58 also interacts with ADRP (perilipin-2) and co-localizes with ADRP-coated lipid droplets in non-differentiated cells. Yeast two-hybrid, GFP fusion co-localization, loss-of-function CDS mutants The Journal of biological chemistry Medium 15136565
2007 CGI-58 knockdown in 3T3-L1 preadipocytes and Hepa1 hepatoma cells causes abnormal LD accumulation and reduces basal and PKA-stimulated lipolysis. In vitro, CGI-58 itself lacks lipase/esterase activity but enhances ATGL activity. Upon lipolytic stimulation, CGI-58 disperses from LDs to the cytosol, dependent on perilipin phosphorylation (phosphorylated perilipin loses CGI-58 binding). siRNA knockdown, in vitro lipase assay, lipolysis assays, live-cell imaging of CGI-58 redistribution Journal of lipid research High 17308334
2008 Recombinant human CGI-58, purified from E. coli, catalyzes acyl-CoA-dependent acylation of lysophosphatidic acid (LPA) to phosphatidic acid (PA). The enzyme does not acylate other lysophospholipids or neutral glycerolipid acceptors. Overexpression of CGI-58 in yeast increases PA and total phospholipids while reducing TG levels. Endogenous CGI-58 is the LPA acyltransferase in mouse white adipose tissue lipid droplets. Recombinant protein purification from E. coli, in vitro acyltransferase assay, overexpression in S. cerevisiae, immunoblot and mass spectrometry in mouse adipose tissue The Journal of biological chemistry High 18606822
2009 Perilipin (Plin) binds ABHD5 with high affinity and sequesters it, thereby suppressing ABHD5 interaction with ATGL and reducing basal lipolysis. PKA-mediated phosphorylation of Plin on Ser492 or Ser517 rapidly releases ABHD5 from Plin, allowing ABHD5 to directly interact with ATGL predominantly on lipid droplets containing Plin. FRET/protein trafficking in live cells (3T3-L1 adipocytes), bimolecular fluorescence complementation, phosphorylation site mutagenesis The Journal of biological chemistry High 19850935
2009 Recombinant mouse CGI-58 expressed in E. coli displays acyl-CoA-dependent lysophosphatidic acid acyltransferase (LPAAT) activity, with preference for arachidonoyl-CoA and oleoyl-CoA as acyl donors and 1-oleoyl-LPA as acceptor. CGI-58 contains a conserved HXXXXD motif consistent with acyltransferase function. Expression of CGI-58 in CDS fibroblasts increases incorporation of fatty acids released from stored TG into phospholipids. Recombinant protein expression in E. coli, in vitro LPAAT assay with substrate specificity, fluorescence quenching, radiotracer lipid incorporation in fibroblasts Journal of lipid research High 19801371
2009 CGI-58-deficient (Cgi-58−/−) mice display systemic TG accumulation, severe hepatic steatosis, and a lethal neonatal skin permeability barrier defect. The skin barrier defect is linked to impaired epidermal TG hydrolysis and consequent failure to synthesize acylceramides, revealing an ATGL-independent function of CGI-58 in skin lipid metabolism. Constitutive mouse knockout, lipid analysis, histology, metabolic measurements The Journal of biological chemistry High 20023287
2008 ABHD5 interacts with Mldp (LSDP5/PLIN5) on the surface of lipid droplets in cardiac muscle, directing ABHD5 to those droplets in proportion to Mldp concentration. An ABHD5 E262K mutant with reduced Mldp binding fails to support Atgl activity at Mldp-containing lipid droplets, despite Atgl being present, demonstrating that the ABHD5-Mldp interaction is required for Atgl activation in this context. Co-IP in situ, fluorescence co-localization in cardiac muscle fibers and transfected fibroblasts, point-mutant ABHD5 E262K functional analysis, oleic acid loading, lipid droplet assays The Journal of biological chemistry High 19064991
2010 The N-terminal tryptophan-rich region (aa 1-30) of CGI-58 is required for lipid droplet binding and for ATGL activation. NMR experiments demonstrate strong interaction between the N-terminal peptide and dodecylphosphocholine micelles (lipid droplet mimic). N-terminally truncated CGI-58 localizes to the cytoplasm and loses ability to stimulate ATGL, linking correct localization to activating function. 1H NMR with lipid-droplet-mimicking micelles, GFP-fusion localization, deletion mutants in cell culture, ATGL activation assays The Journal of biological chemistry High 20164531
2011 Human PLIN1 C-terminal frameshift mutations (Leu-404fs, Val-398fs) fail to bind ABHD5, causing constitutive ABHD5-mediated coactivation of ATGL and elevated basal lipolysis. siRNA knockdown of either ABHD5 or ATGL in cells expressing mutant PLIN1 reduces basal lipolysis, placing ABHD5 between PLIN1 and ATGL in the lipolytic signaling hierarchy. Bimolecular fluorescence complementation (BiFC), siRNA knockdown, basal lipolysis assay in preadipocytes The Journal of biological chemistry High 21757733
2011 The minimal active domain of ATGL (aa 1-254) retains both TG hydrolase activity and the capacity to be coactivated by CGI-58 and inhibited by G0S2, establishing that the CGI-58 interaction interface is within this minimal patatin-domain fragment. G0S2 inhibits ATGL independently of CGI-58 and regardless of ATGL activity state. Domain truncation, in vitro TG hydrolase assay, co-IP with CGI-58 and G0S2, 3D homology modeling PloS one Medium 22039468
2014 CGI-58 is phosphorylated by PKA on Ser239 in mouse (Ser237 in human). Phosphorylation of Ser239 is required for dispersion of CGI-58 from PLIN1-coated lipid droplets upon PKA activation, thereby increasing CGI-58 availability for ATGL coactivation. Phosphorylation of CGI-58 itself neither increases nor impairs in vitro ATGL coactivation; perilipin phosphorylation also contributes to CGI-58 dispersion. Phosphoamino acid analysis, mass spectrometry, immunoblotting of recombinant and endogenous CGI-58, S239A/S240A mutagenesis, subcellular localization in adipocytes, in vitro ATGL coactivation assay Journal of lipid research High 25421061
2015 Synthetic ligands directly bind ABHD5 (confirmed by affinity probe labeling and molecular imaging), releasing ABHD5 from PLIN1 or PLIN5 without PKA activation, thereby rapidly activating adipocyte and muscle lipolysis. Endogenous ligands including long-chain acyl-CoA also regulate ABHD5-PLIN interactions. Synthetic ligand screen, affinity probe labeling, molecular imaging (FRET/BiFC), lipolysis assays in 3T3-L1 adipocytes and muscle cells Cell metabolism High 26411340
2015 The NMR solution structure of the CGI-58 N-terminal lipid-droplet anchor peptide (residues 10-31) bound to DPC micelles reveals that Trp21/Trp25 form one anchor arm and Trp29 forms an independent second arm. Simultaneous Trp-to-Ala substitutions in both arms abolish CGI-58 lipid droplet localization and ATGL-activating function, while single-arm substitutions do not. Solution NMR structure of N-terminal peptide with DPC micelles, Trp-to-Ala mutagenesis, cell-based localization and ATGL activation assays The Journal of biological chemistry High 26350461
2014 Perilipin 1 C-terminus binds ABHD5 and stabilizes it by retarding its proteasomal degradation; perilipins 2 and 3 lack this C-terminal domain and thus sequester ABHD5 less effectively, resulting in higher rates of basal lipolysis in non-adipose tissues. Chimeric proteins with PLIN1 C-terminus fused to PLIN2/3 N-terminus stabilize ABHD5 and suppress basal lipolysis. BiFC assays, chimeric perilipin constructs, perilipin knockdown in adipocytes, proteasome inhibition experiments, basal lipolysis measurement Proceedings of the National Academy of Sciences of the United States of America High 24927580
2016 Two conserved ABHD5 residues (R299 and G328) are required for ATGL activation. Introducing equivalent residues into the paralog ABHD4 (N303R/S332G) confers ATGL-activating ability. Corresponding mutations in ABHD5 (R299N, G328S) selectively disrupt lipolysis without affecting ATGL lipid droplet translocation, PLIN binding, or ligand interactions, defining a novel functional surface on ABHD5 for lipase activation. Comparative evolutionary analysis, gain-of-function mutagenesis of ABHD4, loss-of-function mutagenesis of ABHD5, ATGL activation assays in Cos7 cells/brown adipocytes/artificial lipid droplets, structural modeling Scientific reports High 28211464
2018 ABHD5 directly interacts with PNPLA1 and recruits it to lipid droplets, stimulating PNPLA1-catalyzed ω-O-acylceramide (AcylCer) biosynthesis essential for skin barrier formation. ABHD5 mutations associated with ichthyosis in Chanarin-Dorfman syndrome fail to accelerate PNPLA1-mediated AcylCer production. Co-expression in AcylCer-producing cell system, immunofluorescence and immunoelectron microscopy, loss-of-function CDS mutants, lipid analysis Journal of lipid research High 30361410
2018 ABHD5 stimulates PNPLA1-catalyzed acylceramide synthesis; co-expression causes PNPLA1 to relocalize from dispersed to lipid-droplet membranes, and at high expression levels leads to lipid droplet morphological transformation into vesicles or ER incorporation. CDS-associated ABHD5 mutations reduce this ability. Indirect immunofluorescence microscopy, immunoelectron microscopy, acylceramide production assay in HeLa cells, CDS mutant analysis Journal of dermatological science Medium 30527376
2019 ABHD5 functions as a serine protease that cleaves HDAC4 in vitro and in vivo, generating an N-terminal HDAC4 polypeptide (HDAC4-NT) that inhibits MEF2-dependent gene expression and controls glucose handling. ABHD5 deficiency leads to cardiac lipid accumulation; cardiac gene therapy with HDAC4-NT prevents heart failure without preventing lipid accumulation, separating lipotoxicity from functional cardiac protection. In vitro proteolysis assay, in vivo mouse cardiac gene therapy, MEF2 reporter assay, pressure-overload heart failure model, ABHD5 overexpression in transgenic mice Nature metabolism High 31742248
2019 PNPLA3 (WT and I148M) interacts directly with CGI-58; co-immunoprecipitation and pulldown with purified proteins from mouse livers confirm this interaction. PNPLA3 requires CGI-58 for its localization to hepatic lipid droplets, and overexpression of PNPLA3(148M) increases hepatic TG in WT but not in liver-specific Cgi-58 KO mice, establishing that the pro-steatotic effect of PNPLA3(148M) requires CGI-58. Co-immunoprecipitation in mouse livers, in vitro pulldown with purified proteins, liver-specific CGI-58 KO mice, CGI-58 dependent PNPLA3 localization Hepatology High 30802989
2016 CGI-58 knockdown causes hepatic steatosis in mice both with and without ATGL, demonstrating that CGI-58 regulates hepatic TG and diacylglycerol accumulation, and hepatic inflammation, via ATGL-independent mechanisms. ATGL deficiency (but not CGI-58 deficiency) suppresses the hepatic de novo lipogenic program. Mice with single and double deficiency of CGI-58 and ATGL (direct genetic comparison), lipid analysis, gene expression profiling Cell reports High 27396333
2013 CGI-58 knockdown in mice sequesters diacylglycerols (DAG) in lipid droplets/ER rather than the plasma membrane, preventing PKCε translocation to the plasma membrane and thereby dissociating DAG accumulation from hepatic insulin resistance. Antisense oligonucleotide knockdown in mice, hyperinsulinemic-euglycemic clamp, subcellular DAG fractionation, PKCε membrane translocation assay Proceedings of the National Academy of Sciences of the United States of America High 23302688
2016 ABHD5 directly interacts with BECN1 (Beclin 1) and competes with caspase-3 (CASP3) for binding at BECN1 cleavage sites, preventing CASP3-mediated BECN1 cleavage and inactivation, thereby sustaining autophagic flux. ABHD5 deficiency permits CASP3 to cleave BECN1, impairing autophagy independent of PNPLA2/ATGL. Co-IP, competitive binding assay, autophagic flux measurement, CASP3 cleavage assay, colorectal cancer cell lines and intestine-specific KO mouse model Autophagy Medium 27559856
2016 Macrophage ABHD5 suppresses spermidine synthase (SRM)-dependent spermidine production by inhibiting ROS-dependent expression of C/EBPε, which activates SRM transcription. ABHD5 expression in macrophages thereby reduces spermidine availability and potentiates CRC growth; additional SRM transgene in macrophages prevents ABHD5 transgene-induced CRC growth. In vitro macrophage-CRC co-culture, mouse xenograft and genetic cancer models, SRM transgene rescue experiment, ROS measurement, C/EBPε expression analysis Nature communications High 27189574
2021 ABHD5 interacts in the cytoplasm with DPY30 (core subunit of SET1A methyltransferase complex), inhibiting DPY30 nuclear translocation and SET1A activity. ABHD5 loss allows DPY30 nuclear entry, enabling SET1A-mediated methylation of YAP and histone H3, sequestering YAP in the nucleus and promoting c-Met transcription to sustain CRC stemness. Co-IP for ABHD5-DPY30 interaction, nuclear fractionation, SET1A methyltransferase assay, YAP methylation assay, gene expression analysis, CRC cell and mouse models Nature communications High 34795238
2020 ABHD5-mediated lipolysis activates the AMPK/mTORC1 pathway by elevating intracellular AMP, leading to AMPK activation and mTORC1 inhibition, suppressing protein synthesis and cancer cell growth. This suppression requires fatty acid re-esterification (by DGAT1/DGAT2), which consumes ATP, creating a futile cycle between TG hydrolysis and resynthesis. ABHD5 overexpression and pharmacological lipolysis activation, AMP/ATP measurement, AMPK/mTORC1 signaling assays, DGAT1/2 inhibition, cell cycle analysis in prostate cancer cells The Journal of biological chemistry Medium 33219129
2014 Recombinant CGI-58 catalyzes reacylation of lysophosphatidylglycerol to phosphatidylglycerol (PG) in an acyl-CoA-dependent manner, but lacks acyltransferase activity toward other lysophospholipids. Overexpression and knockdown of CGI-58 in C2C12 cells reciprocally affect endogenous PG levels, thereby altering cardiolipin availability and mitochondrial autophagy (mitophagy) through PINK1/AMPK/mTORC1 signaling. Recombinant protein from Sf9 cells, in vitro acyltransferase assay with substrate panel, overexpression/knockdown in C2C12 cells, lipid analysis, mitophagy and autophagy assays The Journal of biological chemistry Medium 25315780
2020 ABHD5 cooperates with ATGL to mobilize lipid droplet-stored triglycerides required for HCV infectious particle production in hepatocytes. Specific ABHD5 residues critical for ATGL activation are required for both lipolytic and pro-viral functions; grafting these ABHD5 residues onto the paralog ABHD4 confers pro-viral and lipolytic activity. ABHD5 residues at the predicted ATGL interface are necessary for both functions. ATGL modulation (protein expression and lipase inhibitor), ABHD4 gain-of-function mutagenesis, ABHD5 loss-of-function mutagenesis, HCV production assay, lipid droplet lipolysis measurement PLoS pathogens High 32542055
2014 Macrophage-specific CGI-58 knockout causes mitochondrial dysfunction via defective PPARγ signaling, leading to ROS overproduction that activates NLRP3 inflammasome, potentiating proinflammatory cytokine secretion and aggravating HFD-induced insulin resistance. Anti-ROS treatment or NLRP3 silencing prevents cytokine oversecretion and insulin resistance in CGI-58-deficient macrophages. Macrophage-specific CGI-58 KO mice, mitochondrial function assays, ROS measurement, NLRP3 inflammasome activation, anti-ROS treatment, cytokine assays, co-culture with fat slices Cell reports High 24703845
2008 CGI-58 is localized to lamellar granules in differentiated keratinocytes of the granular layer. CGI-58 knockdown reduces expression of keratinocyte differentiation/keratinization markers, indicating a role in keratinocyte differentiation and lamellar granule lipid metabolism for skin barrier formation. Immunoelectron microscopy of lamellar granules, immunohistochemistry of human epidermis, siRNA knockdown in cultured keratinocytes, organotypic 3D cultures The American journal of pathology Medium 18832586
2025 Lipid droplet targeting of ABHD5 is required for its interaction with PNPLA3 I148M. Fluorescence cross-correlation spectroscopy demonstrates that PNPLA3 I148M has greater association with ABHD5 on LDs than WT PNPLA3. PNPLA3 C-terminus is sufficient for LD targeting and ABHD5 interaction. LD targeting of PNPLA3 I148M is required to promote steatosis in vitro and in vivo. Fluorescence cross-correlation spectroscopy, molecular modeling, C-terminal domain truncation, in vitro steatosis assay, in vivo liver steatosis model The Journal of biological chemistry Medium 39814233
2010 A short CGI-58 splice isoform (mCGI-58S), lacking exons 2 and 3, localizes predominantly to the cytoplasm (not lipid droplets), cannot activate ATGL, cannot promote lipid droplet turnover, but retains LPA acyltransferase activity, functionally dissociating ATGL activation from acyltransferase function. Cloning of alternative splice variant, GFP-fusion localization, ATGL activation assay, lipid droplet accumulation assay, LPA acyltransferase 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 743 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 380 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 314 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 216 15136565
2019 PNPLA3, CGI-58, and Inhibition of Hepatic Triglyceride Hydrolysis in Mice. Hepatology (Baltimore, Md.) 181 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 158 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 138 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 134 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 112 18606822
2015 Endogenous and Synthetic ABHD5 Ligands Regulate ABHD5-Perilipin Interactions and Lipolysis in Fat and Muscle. Cell metabolism 103 26411340
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.) 97 20676045
2014 Macrophage CGI-58 deficiency activates ROS-inflammasome pathway to promote insulin resistance in mice. Cell reports 86 24703845
2014 Loss of abhd5 promotes colorectal tumor development and progression by inducing aerobic glycolysis and epithelial-mesenchymal transition. Cell reports 86 25482557
2016 Macrophage ABHD5 promotes colorectal cancer growth by suppressing spermidine production by SRM. Nature communications 83 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 75 14708602
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 61 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
2021 ABHD5 inhibits YAP-induced c-Met overexpression and colon cancer cell stemness via suppressing YAP methylation. Nature communications 56 34795238
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
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
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 47 30527376
2015 Structure of a CGI-58 motif provides the molecular basis of lipid droplet anchoring. The Journal of biological chemistry 47 26350461
2018 ABHD5 stimulates PNPLA1-mediated ω-O-acylceramide biosynthesis essential for a functional skin permeability barrier. Journal of lipid research 46 30361410
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
2020 The ATGL lipase cooperates with ABHD5 to mobilize lipids for hepatitis C virus assembly. PLoS pathogens 38 32542055
2015 ATGL and CGI-58 are lipid droplet proteins of the hepatic stellate cell line HSC-T6. Journal of lipid research 36 26330055
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 28 27124600
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 28 25381252
2009 ABHD5/CGI-58 facilitates the assembly and secretion of apolipoprotein B lipoproteins by McA RH7777 rat hepatoma cells. Biochimica et biophysica acta 28 19211039
2014 Deletion of CGI-58 or adipose triglyceride lipase differently affects macrophage function and atherosclerosis. Journal of lipid research 27 25316883
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 25 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
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 18 28827091
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
2015 Muscle-specific deletion of comparative gene identification-58 (CGI-58) causes muscle steatosis but improves insulin sensitivity in male mice. Endocrinology 17 25751639
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
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
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 12 39814233
2022 ABHD5 frameshift deletion in Golden Retrievers with ichthyosis. G3 (Bethesda, Md.) 12 34791225
2013 Acitretin-responsive ichthyosis in Chanarin-Dorfman syndrome with a novel mutation in the ABHD5/CGI-58 gene. Pediatric dermatology 12 23756328
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
2024 HBB contributes to individualized aconitine-induced cardiotoxicity in mice via interfering with ABHD5/AMPK/HDAC4 axis. Acta pharmacologica Sinica 10 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 10 36107452
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
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
2021 circFAM120A participates in repeated implantation failure by regulating decidualization via the miR-29/ABHD5 axis. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 7 34449947
2020 Transcription Factors ZEB1 and CREB Promote the Transcription of Bovine ABHD5 Gene. DNA and cell biology 7 33332227
2014 Transgenic CGI-58 expression in macrophages alleviates the atherosclerotic lesion development in ApoE knockout mice. Biochimica et biophysica acta 7 25178844

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