Affinage

AGPAT2

1-acyl-sn-glycerol-3-phosphate acyltransferase beta · UniProt O15120

Length
278 aa
Mass
30.9 kDa
Annotated
2026-06-09
45 papers in source corpus 17 papers cited in narrative 18 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 5/6 claims corpus-supported (83%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

AGPAT2 is an endoplasmic reticulum-localized 1-acylglycerol-3-phosphate O-acyltransferase that acylates lysophosphatidic acid (LPA) to phosphatidic acid (PA), a central intermediate for triacylglycerol and glycerophospholipid biosynthesis, and its loss-of-function mutations cause congenital generalized lipodystrophy (PMID:11967537, PMID:21873652). The PA pool generated by AGPAT2 serves multiple downstream fates: it is channeled into the CDP-DAG phospholipid synthesis pathway through direct interaction with the CDP-diacylglycerol synthases CDS1/CDS2, whose stability and activity depend on AGPAT2 (PMID:34824276), and it drives ER tubulation by supplying PA to the dynamin-related GTPase DRP1 to remodel ER membrane morphology (PMID:41387688). AGPAT2 is an essential regulator of adipocyte differentiation, acting upstream of PI3K/Akt and PPARγ signaling by tuning levels of PA, LPA, phosphatidylinositol species, and the PPARγ inhibitor cyclic PA (PMID:22872237), and its activity is genetically required for adipose tissue formation and maintenance in vivo (PMID:37752957). At the ER, seipin oligomers physically scaffold AGPAT2 together with lipin 1 to coordinate sequential PA metabolism during adipogenesis (PMID:25737955). Transcriptionally, HIF-1α directly binds an HRE in the AGPAT2 promoter to induce its expression under hypoxia, promoting lipid droplet accumulation and cell survival (PMID:29908837). Misregulation of AGPAT2-derived PA has systemic metabolic consequences, including PA-species-driven hepatic glucose production and insulin resistance (PMID:24425876).

Mechanistic history

Synthesis pass · year-by-year structured walk · 16 steps
  1. 2002 High

    Established the molecular identity and clinical relevance of AGPAT2 by linking its acyltransferase activity to a human disease, answering what the gene does and why its loss matters.

    Evidence Mutation identification in lipodystrophy patients combined with enzymatic function annotation

    PMID:11967537

    Open questions at the time
    • Did not resolve subcellular site of catalysis
    • Did not define which downstream PA pools account for the disease phenotype
  2. 2009 High

    Showed how cells compensate for AGPAT2 loss, revealing activation of an alternative MOGAT1-dependent monoacylglycerol pathway and elevated de novo lipogenesis as a route to triglyceride synthesis.

    Evidence Agpat2 knockout mouse with metabolic flux, gene/protein expression, and dietary intervention

    PMID:19187773

    Open questions at the time
    • Did not establish whether compensation occurs in adipose or only liver
    • Did not link compensatory pathway to lipodystrophy progression
  3. 2011 High

    Defined the biochemical substrate specificity and ER localization of AGPAT2 and showed, via liver-specific rescue failure, that hepatic AGPAT activity is not the primary driver of lipodystrophic steatosis.

    Evidence In vitro acyltransferase assays, co-localization imaging, homology modeling, and adenoviral liver rescue in knockout mice

    PMID:21873652

    Open questions at the time
    • Did not identify the tissue where AGPAT2 activity is essential
    • No experimental structure of AGPAT2
  4. 2012 High

    Placed AGPAT2 upstream of PI3K/Akt and PPARγ in adipogenesis by showing that its lipid products control these signaling pathways, and identified post-translational destabilization as a disease mechanism for specific mutants.

    Evidence Knockdown/overexpression in 3T3-L1 and patient cells, lipidomics, Akt and PPARγ rescue; mutant protein/mRNA quantification and rescue assays

    PMID:22872237 PMID:23430550

    Open questions at the time
    • Did not define which PA/LPA species mediate each signaling step
    • Mechanism connecting lipid changes to Akt activation not resolved
  5. 2014 High

    Connected AGPAT2-related lipid dysregulation to systemic insulin resistance by showing that specific PA species accumulating in its absence drive hepatic glucose production resistant to insulin suppression.

    Evidence Primary hepatocyte assays with defined PA species, gluconeogenic enzyme measurement, and insulin suppression in KO vs WT

    PMID:24425876

    Open questions at the time
    • Did not identify the PA receptor/sensor driving gluconeogenesis
    • Did not separate liver-autonomous from systemic effects
  6. 2015 High

    Revealed how AGPAT2 is spatially organized for adipogenesis, demonstrating that seipin scaffolds AGPAT2 and lipin 1 into a complex that coordinates sequential PA metabolism and promotes PPARγ nuclear accumulation.

    Evidence Co-immunoprecipitation, immunofluorescence, and atomic force microscopy

    PMID:25737955

    Open questions at the time
    • Stoichiometry of the in vivo complex not resolved
    • Did not show PA channeling within the complex directly
  7. 2016 High

    Characterized the cellular and ultrastructural basis of adipose loss in AGPAT2 deficiency, showing postnatal adipocyte death, absent caveolae, abnormal organelles, and elevated PA that PPARγ overexpression cannot rescue.

    Evidence Electron microscopy, phospholipid profiling by ESI-MS/MS, and PPARγ rescue in MEFs

    PMID:27408775

    Open questions at the time
    • Mechanism linking PA elevation to adipocyte death unresolved
    • Cause of caveolae loss not identified
  8. 2018 High

    Identified hypoxia-driven transcriptional control of AGPAT2 by HIF-1α and tied this to lipid droplet accumulation and survival, expanding AGPAT2's role beyond adipogenesis into stress responses.

    Evidence HIF-1α knockdown, AGPAT2 promoter-HRE reporters, ChIP, HRE mutagenesis, lipid droplet and viability assays

    PMID:29908837

    Open questions at the time
    • Did not establish tissue contexts where this axis operates
    • Did not link HIF-driven AGPAT2 to tumor lipid metabolism in vivo
  9. 2018 Medium

    Provided direct enzymatic evidence that compound missense mutations abolish AGPAT2 catalytic activity and associate with partial lipodystrophy, refining genotype-function correlation.

    Evidence In vitro mass spectrometry activity assay and whole genome sequencing in a patient case

    PMID:30319454

    Open questions at the time
    • Single patient case without independent replication
    • Did not separate contributions of each mutation
  10. 2020 Medium

    Extended the seipin scaffolding model upstream by showing seipin can also bind GPAT3 and simultaneously engage AGPAT2, implying a trimeric platform for sequential glycerophospholipid synthesis in adipogenesis.

    Evidence Co-immunoprecipitation, siRNA knockdown, and adipogenesis assays in cultured cells

    PMID:32094408

    Open questions at the time
    • Trimeric complex inferred rather than directly demonstrated
    • Stoichiometry and assembly order not resolved
  11. 2021 High

    Resolved the paradox of PA accumulation in AGPAT2 deficiency by showing AGPAT2 directly binds and stabilizes CDS1/CDS2 to channel PA into the CDP-DAG pathway, so its loss collapses downstream PA consumption.

    Evidence Reciprocal Co-IP, lipidomics, CDS activity assays, and knockout models in cells and mouse liver

    PMID:34824276

    Open questions at the time
    • Structural basis of AGPAT2-CDS interaction not determined
    • Did not quantify substrate channeling kinetics
  12. 2021 Medium

    Dissected the caveolae defect in AGPAT2-null adipocytes, excluding cholesterol, sphingolipid, and caveolin/cavin protein changes and implicating elevated plasma membrane phosphatidylserine.

    Evidence Plasma membrane fractionation, lipidomics, electron microscopy, and immunoblotting

    PMID:33989739

    Open questions at the time
    • Causal role of phosphatidylserine in caveolae loss not proven
    • Did not connect caveolae loss to adipocyte function
  13. 2023 High

    Established AGPAT2 as causally required for adipocyte differentiation in vivo through reversible adipose-specific re-expression that regenerates adipose tissue and is lost when expression is switched off.

    Evidence Doxycycline-inducible adipose-specific transgene in Agpat2-null mice with histology, leptin, and ex vivo differentiation

    PMID:37752957

    Open questions at the time
    • Did not identify the minimal AGPAT2-dependent lipid signal for differentiation
    • Partial regeneration mechanism not fully defined
  14. 2025 High

    Uncovered a structural role for AGPAT2-generated PA in organelle morphogenesis, showing PA is supplied to DRP1 to drive ER tubulation independently of DRP1 GTP hydrolysis, with PA reduction converting tubules into sheets.

    Evidence Knockout, FIB-SEM, super-resolution microscopy, lipidomics, AlphaFold modeling, in vitro ER tubulation reconstitution and activity assays, LIPIN1 expression

    PMID:41387688

    Open questions at the time
    • Did not define how local PA pools are spatially restricted at ER tubules
    • Physiological consequences of altered ER morphology in lipodystrophy not assessed
  15. 2026 Medium

    Revealed a nuclear pore complex pool of AGPAT2 under mTOR/Dop1a control that gates nuclear membrane phospholipid synthesis and prevents nuclear lipid droplet formation when LPA is limiting.

    Evidence NPC localization studies, Dop1a knockout/rescue, mTOR perturbation, and nuclear lipid droplet and phospholipid measurements

    PMID:42164854

    Open questions at the time
    • Single lab with limited replication of NPC localization
    • Molecular details of Dop1a-AGPAT2 inhibition not structurally defined
  16. 2026 Medium

    Demonstrated that pharmacological AGPAT2/LPAAT-β inhibition imposes G2/M arrest and caspase-independent necrotic death, including in bortezomib-resistant cells, indicating a role in cell cycle and survival exploitable therapeutically.

    Evidence CT-32615 inhibition with cell cycle analysis, caspase/PARP assays, and viability in resistant lines

    PMID:15735676

    Open questions at the time
    • Relies on inhibitor specificity for AGPAT2
    • Mechanism linking AGPAT2 activity to cdc25c/cdc2 downregulation not established

Open questions

Synthesis pass · forward-looking unresolved questions
  • How AGPAT2-generated PA is spatially partitioned among its distinct fates — CDS-mediated phospholipid synthesis, DRP1-driven ER tubulation, signaling pools regulating adipogenesis, and nuclear membrane biogenesis — remains unresolved.
  • No experimental structure of AGPAT2 or its protein complexes
  • No mechanism explaining selective channeling of PA into competing downstream pathways
  • Tissue-specific regulation of the distinct AGPAT2 functions undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0016740 transferase activity 4
Localization
GO:0005783 endoplasmic reticulum 2 GO:0005635 nuclear envelope 1
Pathway
R-HSA-1430728 Metabolism 3 R-HSA-1266738 Developmental Biology 2 R-HSA-1852241 Organelle biogenesis and maintenance 1
Partners
BSCL2CDS1CDS2DOP1ADRP1GPAT3LPIN1
Complex memberships
AGPAT2–CDS1/CDS2 complexseipin–AGPAT2–lipin 1 scaffold complex

Evidence

Reading pass · 18 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2002 AGPAT2 encodes a 1-acylglycerol-3-phosphate O-acyltransferase that catalyzes the acylation of lysophosphatidic acid (LPA) to form phosphatidic acid (PA), a key intermediate in the biosynthesis of triacylglycerol and glycerophospholipids; loss-of-function mutations cause congenital generalized lipodystrophy. Mutation identification in human patients combined with enzymatic function annotation of the AGPAT2 protein Nature genetics High 11967537
2011 Human AGPAT2 and AGPAT1 show similar in vitro substrate specificities for LPA and acyl-CoA; both co-localize to the endoplasmic reticulum when co-expressed; protein homology modeling with GPAT1 reveals similar tertiary structure consistent with substrate specificity. In vitro enzymatic assays with LPA and acyl-CoA substrates, co-localization by fluorescence microscopy, protein homology modeling The Journal of biological chemistry High 21873652
2011 Restoring AGPAT2 activity specifically in the liver by adenoviral overexpression of AGPAT1 or AGPAT2 in Agpat2-/- mice failed to ameliorate hepatic steatosis, indicating that liver-specific AGPAT activity is not the primary driver of hepatic fat accumulation in lipodystrophy. Adenoviral gene delivery to liver of Agpat2-/- mice followed by measurement of liver triglycerides The Journal of biological chemistry Medium 21873652
2009 In Agpat2-/- mice, hepatic de novo fatty acid biosynthesis is increased ~4-fold and monoacylglycerol acyltransferase isoform 1 (MOGAT1) mRNA and protein are markedly upregulated, indicating activation of an alternative monoacylglycerol pathway for triglyceride biosynthesis to compensate for AGPAT2 deficiency. Agpat2 knockout mouse model; de novo lipogenesis rates measured; mRNA and protein analysis of MOGAT1; fat-free diet intervention Cell metabolism High 19187773
2015 Seipin oligomers (dodecamers) can directly interact with AGPAT2 during adipogenesis, and a single seipin complex can simultaneously bind both AGPAT2 and lipin 1, physically scaffolding these two sequential enzymes of the PA biosynthesis pathway; stabilizing the seipin-AGPAT2 interaction increases nuclear accumulation of PPARγ. Co-immunoprecipitation, immunofluorescence, atomic force microscopy (AFM) to determine direct protein-protein interaction and molecular architecture Molecular metabolism High 25737955
2012 AGPAT2 regulates adipogenesis by modulating levels of phosphatidic acid, lysophosphatidic acid, phosphatidylinositol species, and the PPARγ inhibitor cyclic phosphatidic acid; loss of AGPAT2 activity reduces Akt activation, and constitutively active Akt partially restores lipogenesis, placing AGPAT2 upstream of PI3K/Akt and PPARγ pathways in early adipogenesis. Knockdown and overexpression of AGPAT2 in 3T3-L1 and patient-derived MDMCs; lipidomics; retroviral rescue; constitutively active Akt rescue; PPARγ agonist rescue Diabetes High 22872237
2014 Specific molecular species of phosphatidic acid (PA C16:0/18:1 and C18:1/20:4) generated in the absence of AGPAT2 enhance hepatic glucose production (HGP) in primary hepatocytes by upregulating gluconeogenic enzymes glucose-6-phosphatase and PEPCK; this PA-driven gluconeogenesis is suppressed by insulin in wild-type but not Agpat2-/- hepatocytes, establishing PA as a driver of hepatic insulin resistance. Primary hepatocyte assays with exogenous PA species; measurement of glucose production; diacylglycerol kinase and phospholipase D activity assays in Agpat2-/- liver; insulin suppression experiments The Journal of biological chemistry High 24425876
2021 AGPAT2 directly interacts with CDP-diacylglycerol synthases (CDS1 and CDS2), forming functional complexes that promote flux of PA into the CDP-DAG phospholipid synthesis pathway; AGPAT2 deficiency destabilizes CDS proteins and reduces CDS activity, paradoxically increasing PA levels despite AGPAT2 producing PA. Co-immunoprecipitation, lipidomics, CDS activity assays in cell lines and mouse liver, knockout models Nature communications High 34824276
2016 AGPAT2 deficiency causes postnatal loss of both white and brown adipose tissue through adipocyte death and local inflammation during the first postnatal week; Agpat2-/- adipocytes are virtually devoid of caveolae, have abnormal mitochondria and lipid droplets, and show 3-fold elevated phosphatidic acid in phospholipid composition; PPARγ overexpression increases differentiation but does not rescue morphological abnormalities or cell death. Light and electron microscopy of adipose tissue, phospholipid profiling by ESI-MS/MS, PPARγ overexpression rescue in MEFs, immunoblot and qPCR Molecular metabolism High 27408775
2018 AGPAT2 gene expression is directly regulated by HIF-1 transcription factor; HIF-1α binds a specific HRE in the AGPAT2 promoter (confirmed by ChIP), and mutation of this HRE abolishes hypoxic activation; AGPAT2 knockdown reduces lipid droplet accumulation and cell viability under hypoxia and increases sensitivity to etoposide. siRNA knockdown of HIF-1α; reporter gene assays with AGPAT2 promoter-HRE constructs; chromatin immunoprecipitation (ChIP); HRE mutagenesis; lipid droplet quantification; cell viability assays Biochimica et biophysica acta. Molecular and cell biology of lipids High 29908837
2020 Seipin and GPAT3 associate via direct interaction, and seipin can simultaneously bind GPAT3 and AGPAT2, suggesting a trimeric complex that co-ordinates sequential steps of the glycerophospholipid pathway; inhibition of AGPAT2 or GPAT3 individually impairs early adipocyte differentiation markers. Co-immunoprecipitation, siRNA knockdown of seipin/AGPAT2/GPAT3, adipogenesis assays in cultured cells Scientific reports Medium 32094408
2012 The p.Cys48Arg and p.Leu228Pro AGPAT2 mutations result in significantly reduced protein levels despite normal mRNA levels (post-translational destabilization); these mutants fail to rescue adipogenesis in AGPAT2-deficient preadipocytes, whereas wild-type AGPAT2 partially rescues differentiation. Expression of mutant vs wild-type AGPAT2 in AGPAT2-deficient preadipocytes; mRNA and protein quantification; adipogenesis rescue assay JIMD reports Medium 23430550
2018 A double-mutant AGPAT2 protein (V67M;V167A) is enzymatically inactive as measured by in vitro mass spectrometry-based activity assay, and is associated with partial lipodystrophy when present as a single complex allele. In vitro enzymatic activity assay with mass spectrometry readout; whole genome sequencing for allele identification Frontiers in physiology Medium 30319454
2023 Adipose-tissue-specific re-expression of human AGPAT2 in Agpat2-null mice under doxycycline regulation results in partial regeneration of white and brown adipose tissue with molecular adipocyte signatures and leptin secretion; turning off AGPAT2 expression causes total loss of regenerated adipose tissue, establishing AGPAT2 as essential for adipocyte differentiation in vivo. Doxycycline-inducible adipose-specific transgene expression in Agpat2-null mice; adipose tissue mass, histology, leptin secretion measurement; ex vivo differentiation of stromal vascular fraction cells iScience High 37752957
2025 AGPAT2-generated phosphatidic acid (PA) drives ER tubulation by directly interacting with and supplying PA to the dynamin-related GTPase DRP1, which subsequently tubulates the ER independently of GTP hydrolysis and oligomerization; reduction of PA by ectopic LIPIN1 expression converts ER tubules into sheets, establishing AGPAT2 as a critical regulator of ER morphogenesis. Gene knockout, 3D structural analysis by FIB-SEM, super-resolution microscopy, lipidomics, AlphaFold structural modeling, in vitro reconstitution of ER tubulation, in vitro AGPAT2 activity assay, LIPIN1 ectopic expression Nature communications High 41387688
2026 AGPAT2 localizes to nuclear pore complexes (NPCs) where it is bound and inhibited by Dop1a under mTOR signaling control to regulate phospholipid abundance in nuclear membranes; when LPA is limiting, Dop1a rapidly translocates to NPCs and suppresses AGPAT2-mediated PA synthesis, preventing formation of nuclear lipid droplets. Localization studies of AGPAT2 at NPCs, Dop1a knockout and rescue, mTOR signaling perturbation, nuclear lipid droplet quantification, nuclear membrane phospholipid measurement iScience Medium 42164854
2026 AGPAT2 inhibitor (LPAAT-β inhibitor CT-32615) triggers G2/M cell cycle arrest via downregulation of cdc25c and cdc2, and induces necrotic cell death (without caspase/PARP cleavage) even in bortezomib-resistant cells. Pharmacological inhibition of LPAAT-β/AGPAT2 with CT-32615; cell cycle analysis; caspase/PARP cleavage assays; cell viability assays in resistant cell lines Oncogene Medium 15735676
2021 Decreased caveolae in Agpat2-/- adipocytes are not associated with changes in plasma membrane cholesterol or sphingolipid levels, nor with changes in caveolin-1 or cavin-1 protein levels; however, increased plasma membrane phosphatidylserine is detected in Agpat2-/- adipocytes at day 10 of differentiation, suggesting a possible role for this lipid in caveolae reduction. Plasma membrane purification by ultracentrifugation; sterol, sphingolipid, and phospholipid lipidomics; caveolae quantification by electron microscopy; immunoblot for caveolin-1 and cavin-1 Biochimica et biophysica acta. Molecular basis of disease Medium 33989739

Source papers

Stage 0 corpus · 45 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 AGPAT2 is mutated in congenital generalized lipodystrophy linked to chromosome 9q34. Nature genetics 395 11967537
2009 Molecular mechanisms of hepatic steatosis and insulin resistance in the AGPAT2-deficient mouse model of congenital generalized lipodystrophy. Cell metabolism 187 19187773
2003 Phenotypic heterogeneity in body fat distribution in patients with congenital generalized lipodystrophy caused by mutations in the AGPAT2 or seipin genes. The Journal of clinical endocrinology and metabolism 114 14602785
2015 Seipin oligomers can interact directly with AGPAT2 and lipin 1, physically scaffolding critical regulators of adipogenesis. Molecular metabolism 73 25737955
2011 Human 1-acylglycerol-3-phosphate O-acyltransferase isoforms 1 and 2: biochemical characterization and inability to rescue hepatic steatosis in Agpat2(-/-) gene lipodystrophic mice. The Journal of biological chemistry 72 21873652
2018 Expression of AGPAT2, an enzyme involved in the glycerophospholipid/triacylglycerol biosynthesis pathway, is directly regulated by HIF-1 and promotes survival and etoposide resistance of cancer cells under hypoxia. Biochimica et biophysica acta. Molecular and cell biology of lipids 69 29908837
2003 Prevalence of mutations in AGPAT2 among human lipodystrophies. Diabetes 66 12765973
2012 Alterations in lipid signaling underlie lipodystrophy secondary to AGPAT2 mutations. Diabetes 50 22872237
2004 Mutations in Gng3lg and AGPAT2 in Berardinelli-Seip congenital lipodystrophy and Brunzell syndrome: phenotype variability suggests important modifier effects. The Journal of clinical endocrinology and metabolism 50 15181077
2013 Leptin ameliorates insulin resistance and hepatic steatosis in Agpat2-/- lipodystrophic mice independent of hepatocyte leptin receptors. Journal of lipid research 46 24293639
2005 Molecular characterization of PS-341 (bortezomib) resistance: implications for overcoming resistance using lysophosphatidic acid acyltransferase (LPAAT)-beta inhibitors. Oncogene 41 15735676
2021 AGPAT2 interaction with CDP-diacylglycerol synthases promotes the flux of fatty acids through the CDP-diacylglycerol pathway. Nature communications 38 34824276
2016 AGPAT2 is essential for postnatal development and maintenance of white and brown adipose tissue. Molecular metabolism 38 27408775
2009 Novel mutations of the BSCL2 and AGPAT2 genes in 10 families with Berardinelli-Seip congenital generalized lipodystrophy syndrome. Clinical endocrinology 36 19226263
2004 Mutations in the seipin and AGPAT2 genes clustering in consanguineous families with Berardinelli-Seip congenital lipodystrophy from two separate geographical regions of Brazil. The Journal of clinical endocrinology and metabolism 31 14715872
2010 Pathology of congenital generalized lipodystrophy in Agpat2-/- mice. Veterinary pathology 28 21051554
2020 Oligomers of the lipodystrophy protein seipin may co-ordinate GPAT3 and AGPAT2 enzymes to facilitate adipocyte differentiation. Scientific reports 24 32094408
2020 Congenital Generalized Lipoatrophy (Berardinelli-Seip Syndrome) Type 1: Description of Novel AGPAT2 Homozygous Variants Showing the Highly Heterogeneous Presentation of the Disease. Frontiers in endocrinology 22 32117065
2016 Mogat1 deletion does not ameliorate hepatic steatosis in lipodystrophic (Agpat2-/-) or obese (ob/ob) mice. Journal of lipid research 22 26880786
2005 Phenotypic heterogeneity in biochemical parameters correlates with mutations in AGPAT2 or Seipin genes among Berardinelli-Seip congenital lipodystrophy patients. Journal of inherited metabolic disease 22 16435205
2015 AGPAT2 deficiency impairs adipogenic differentiation in primary cultured preadipocytes in a non-autophagy or apoptosis dependent mechanism. Biochemical and biophysical research communications 20 26417690
2014 Hepatic gluconeogenesis is enhanced by phosphatidic acid which remains uninhibited by insulin in lipodystrophic Agpat2-/- mice. The Journal of biological chemistry 19 24425876
2014 Divergent metabolic phenotype between two sisters with congenital generalized lipodystrophy due to double AGPAT2 homozygous mutations. a clinical, genetic and in silico study. PloS one 16 24498038
2012 Identification of a novel nonsense mutation and a missense substitution in the AGPAT2 gene causing congenital generalized lipodystrophy type 1. European journal of medical genetics 13 22902344
2012 Identification and Characterisation of a Novel Pathogenic Mutation in the Human Lipodystrophy Gene AGPAT2 : C48R: A Novel Mutation in AGPAT2. JIMD reports 11 23430550
2018 Identifying Lysophosphatidic Acid Acyltransferase β (LPAAT-β) as the Target of a Nanomolar Angiogenesis Inhibitor from a Phenotypic Screen Using the Polypharmacology Browser PPB2. ChemMedChem 10 30520265
2018 Further delineation of AGPAT2 and BSCL2 related congenital generalized lipodystrophy in young infants. European journal of medical genetics 8 30266686
2018 A Single Complex Agpat2 Allele in a Patient With Partial Lipodystrophy. Frontiers in physiology 8 30319454
2021 Decreased caveolae in AGPAT2 lacking adipocytes is independent of changes in cholesterol or sphingolipid levels: A whole cell and plasma membrane lipidomic analysis of adipogenesis. Biochimica et biophysica acta. Molecular basis of disease 7 33989739
2020 Leu124Serfs*26, a novel AGPAT2 mutation in congenital generalized lipodystrophy with early cardiovascular complications. Diabetology & metabolic syndrome 7 32280377
2017 Activation of Sphingolipid Pathway in the Livers of Lipodystrophic Agpat2 Mice. Journal of the Endocrine Society 7 29264548
2011 Description of an AGPAT2 pathologic allelic variant in a 54-year-old Caucasian woman with Berardinelli-Seip syndrome. Acta diabetologica 7 21744063
2023 Transcriptional Inhibition of AGPAT2 Induces Abnormal Lipid Metabolism and Oxidative Stress in the Liver of Nile Tilapia Oreochromis niloticus. Antioxidants (Basel, Switzerland) 5 36978948
2023 Lipodystrophic gene Agpat2 deficiency aggravates hyperlipidemia and atherosclerosis in Ldlr-/- mice. Biochimica et biophysica acta. Molecular basis of disease 5 37591406
2023 Regulated adipose tissue-specific expression of human AGPAT2 in lipodystrophic Agpat2-null mice results in regeneration of adipose tissue. iScience 5 37752957
2018 A Patient with Berardinelli-Seip Syndrome, Novel AGPAT2 Splicesite Mutation and Concomitant Development of Non-diabetic Polyneuropathy. Journal of clinical research in pediatric endocrinology 5 30563316
2013 AGPAT2 gene mutation in a child with Berardinelli-Seip congenital lipodystrophy syndrome. Annales d'endocrinologie 5 23337016
2025 The Role of the AGPAT2 Gene in Adipose Tissue Biology and Congenital Generalized Lipodystrophy Pathophysiology. International journal of molecular sciences 3 40508223
2023 Adipose-specific overexpression of human AGPAT2 in mice causes increased adiposity and mild hepatic dysfunction. iScience 3 38274405
2024 Regulated regeneration of adipose tissue in lipodystrophic Agpat2-null mice partially ameliorates hepatic steatosis. iScience 2 38623324
2025 AGPAT2 acts at the crossroads of lipid biosynthesis and DRP1-mediated ER morphogenesis. Nature communications 1 41387688
2024 LncRNA ENSGALG00000021686 regulates fat metabolism in chicken hepatocytes via miR-146b/AGPAT2 pathway. Animal genetics 1 38369771
2026 The mTOR-Dop1a-Agpat2 axis regulates nuclear phospholipid homeostasis. iScience 0 42164854
2025 A case of familial hypertriglyceridemia associated with a novel heterozygous AGPAT2 mutation. Annals of medicine and surgery (2012) 0 40212223
2020 [Identification of a novel AGPAT2 variant in a Chinese patient with congenital generalized lipodystrophy type 1]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics 0 32924125

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