Affinage

APOC2

Apolipoprotein C-II · UniProt P02655

Round 2 corrected
Length
101 aa
Mass
11.3 kDa
Annotated
2026-04-28
64 papers in source corpus 19 papers cited in narrative 19 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

Apolipoprotein C-II is a 78-residue exchangeable apolipoprotein that serves as the obligatory cofactor for lipoprotein lipase (LPL)-mediated hydrolysis of triglycerides in VLDL and chylomicrons. Its C-terminal α-helix (residues 55–78) binds LPL's lid-anchoring regions near the catalytic pocket, increasing LPL thermal stability and protecting against ANGPTL4-induced unfolding, thereby activating triglyceride hydrolysis; the terminal Gly-Glu-Glu residues are critical for this activation (PMID:270715, PMID:37094117). ApoC-II transfers dynamically from HDL to triglyceride-rich lipoproteins during alimentary lipemia, inhibits apoE-dependent hepatic remnant uptake via the LDL receptor pathway, and is transcriptionally induced by FXR in liver and LXR in macrophages (PMID:4345202, PMID:1917954, PMID:11579204, PMID:12032151). Genetic ablation in hamsters causes severe hypertriglyceridemia fully rescued by AAV-delivered human APOC2, and loss of APOC2 in zebrafish additionally impairs LCAT-mediated cholesterol esterification, revealing roles beyond triglyceride catabolism (PMID:32562799, PMID:28107429).

Mechanistic history

Synthesis pass · year-by-year structured walk · 9 steps
  1. 1973 High

    Establishing that apoC-II is not statically bound to one lipoprotein class but dynamically redistributes from HDL to chylomicrons during fat absorption answered how the activator reaches its substrate particles in vivo.

    Evidence Ultracentrifugal fractionation and gel electrophoresis of human lipoproteins pre- and post-fat meal

    PMID:4345202

    Open questions at the time
    • Mechanism governing transfer kinetics and directionality was not defined
    • Whether transfer is passive equilibrium or protein-mediated was not distinguished
  2. 1977 High

    Determination of apoC-II's 78-residue primary structure and mapping of the LPL-activating domain to the C-terminal helix (residues 55–78, with terminal Gly-Glu-Glu essential) resolved which portion of the protein is functionally critical and established the minimal activating unit.

    Evidence Protein sequencing plus in vitro LPL activation assays with synthetic and CNBr-derived peptide fragments

    PMID:194244 PMID:270715

    Open questions at the time
    • Structural basis of how the C-terminal helix contacts LPL was unknown
    • Role of the N-terminal domain in lipid binding versus activation was not separated
  3. 1985 High

    Showing that apoC-II inhibits hepatic uptake of triglyceride-rich lipoprotein remnants—independent of its LPL-activating role—revealed a second function: modulating receptor-mediated clearance by competing with apoE on the particle surface.

    Evidence Perfused rat liver assay with exogenous addition of purified apoC-II to remnant particles; cell-based fibroblast uptake assays with antibody blocking (1991 confirmation)

    PMID:1917954 PMID:4020294

    Open questions at the time
    • Whether inhibition is purely steric displacement of apoE or involves receptor conformational effects was not resolved
    • Relative in vivo contribution of uptake inhibition versus LPL activation to triglyceride homeostasis was not quantified
  4. 2001 High

    Identification of FXR-responsive elements in the apoC-II hepatic control regions and LXR-responsive multienhancers in macrophages established how bile acid and oxysterol signaling transcriptionally control APOC2 expression in distinct cell types.

    Evidence EMSA, luciferase reporters, FXR-null mice with dietary cholic acid (FXR); LXRα/β double-KO macrophages with ligand treatment (LXR)

    PMID:11579204 PMID:12032151

    Open questions at the time
    • Quantitative contribution of FXR versus LXR to circulating apoC-II levels in humans was not determined
    • Post-transcriptional regulation was not addressed
  5. 2001 High

    The discovery that lipid-free apoC-II readily forms amyloid fibrils under physiological conditions—accelerated by macromolecular crowding—raised the question of whether apoC-II amyloidosis occurs in vivo and whether lipid dissociation is a pathogenic event.

    Evidence Thioflavin T fluorescence, turbidity, analytical ultracentrifugation, and quantitative crowding modeling

    PMID:11751863

    Open questions at the time
    • No in vivo evidence that apoC-II amyloid deposits contribute to disease
    • Whether lipoprotein binding constitutively suppresses amyloid nucleation was not tested
  6. 2017 High

    Zebrafish apoc2 knockouts revealed an unexpected requirement for apoC-II in LCAT-mediated cholesterol esterification, extending its metabolic role beyond triglyceride hydrolysis and linking it to HDL maturation.

    Evidence CRISPR apoc2-KO zebrafish with plasma FC/CE ratio measurement, qPCR of lcat/apoA-I, validated in human familial chylomicronemia syndrome patients

    PMID:28107429

    Open questions at the time
    • Whether the cholesterol esterification defect is a direct apoC-II effect or secondary to chronic hypertriglyceridemia was not resolved
    • Mechanism linking apoC-II to lcat transcription was not identified
  7. 2020 High

    CRISPR-generated Apoc2-knockout hamsters confirmed apoC-II as the indispensable LPL cofactor in a mammalian model: severe hypertriglyceridemia was refractory to lipid-lowering drugs but fully corrected by AAV-hApoC2 gene therapy, providing proof-of-concept for gene-replacement treatment.

    Evidence Apoc2-KO hamster model with AAV-hApoC2 rescue, lipid profiling, dietary and pharmacological interventions

    PMID:32562799

    Open questions at the time
    • Long-term safety and durability of AAV-mediated correction were not assessed
    • Effect of gene therapy on cholesterol esterification phenotype was not examined
  8. 2023 High

    HDX-MS revealed the structural mechanism of LPL activation: apoC-II's C-terminal helix binds LPL's lid-anchoring regions overlapping the ANGPTL4 inhibitory site, stabilizing the catalytic pocket against thermal unfolding—explaining why apoC-II and ANGPTL4 act as opposing regulators at the same site.

    Evidence Hydrogen-deuterium exchange mass spectrometry comparing apoC-II and ANGPTL4 binding to LPL, with thermal stability assays

    PMID:37094117

    Open questions at the time
    • Full atomic-resolution co-structure of the apoC-II–LPL complex is not yet available
    • Whether additional LPL-binding partners modulate the apoC-II versus ANGPTL4 competition in vivo is unknown
  9. 2025 Medium

    Placing apoC-II downstream of FXR in beige adipocytes as a promoter of UCP1/PGC1α expression expanded its biology to thermogenesis, while evidence in cancer cells suggested non-canonical JAK-STAT signaling roles, raising the question of whether apoC-II has cell-autonomous signaling functions distinct from lipoprotein metabolism.

    Evidence FXR agonist treatment and siRNA in beige adipocytes with thermogenic marker readouts; APOC2 knockdown in ccRCC cells with p-JAK1/2 and p-STAT3 Western blots and STAT3-agonist rescue

    PMID:39798876 PMID:41296440

    Open questions at the time
    • Whether apoC-II acts as a secreted autocrine/paracrine ligand or intracellularly in these contexts is unknown
    • JAK-STAT activation mechanism—direct receptor engagement versus indirect lipid signaling—is not defined
    • Independent replication of non-canonical signaling roles is needed

Open questions

Synthesis pass · forward-looking unresolved questions
  • A high-resolution co-crystal or cryo-EM structure of the apoC-II–LPL complex is still lacking, the receptor or signaling mechanism underlying apoC-II's reported cell-autonomous effects in non-hepatic tissues remains unidentified, and whether apoC-II amyloid formation has pathological significance in vivo is unresolved.
  • No atomic co-structure of apoC-II–LPL complex
  • No identified receptor for putative cell-autonomous apoC-II signaling
  • In vivo relevance of apoC-II amyloidosis not established

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0048018 receptor ligand activity 3 GO:0098772 molecular function regulator activity 3 GO:0008289 lipid binding 2
Localization
GO:0005576 extracellular region 4 GO:0005811 lipid droplet 1
Pathway
R-HSA-1430728 Metabolism 7 R-HSA-162582 Signal Transduction 3 R-HSA-382551 Transport of small molecules 2
Partners
ABCA1ANGPTL4APOEFXRLCATLPL

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1977 The C-terminal region of apoC-II (residues 55–78) is both necessary and sufficient for maximal activation of lipoprotein lipase (LPL); the fragment 60–78 activates LPL ~4-fold, fragment 55–78 activates ~12-fold (comparable to intact apoC-II at ~13-fold), while removal of the three C-terminal residues (Gly-Glu-Glu) abolishes >95% of activation activity. In vitro LPL activation assay using cyanogen bromide fragments and synthetic peptides of apoC-II Proceedings of the National Academy of Sciences of the United States of America High 270715
1977 ApoC-II has a primary structure of 78 amino acid residues (lacking cysteine, cystine, and histidine), establishing it as the activator protein of LPL in very low density lipoproteins. Protein purification, cyanogen bromide digestion, and sequential amino acid sequencing of tryptic/CNBr peptides Proceedings of the National Academy of Sciences of the United States of America High 194244
1973 During alimentary lipemia, apoC-II (the LPL activator protein) transfers specifically from HDL to chylomicrons, with chylomicron apoC-II concentration directly proportional to particle diameter; HDL apoC-II decreases correspondingly, demonstrating a dynamic exchange of apoC-II between lipoprotein classes. Ultracentrifugal fractionation and polyacrylamide gel electrophoresis of lipoprotein subfractions from human subjects pre- and post-fat meal The Journal of clinical investigation High 4345202
1984 The cDNA for apoC-II was isolated and sequenced, identifying a 22-amino-acid signal peptide and determining relative liver mRNA abundance, establishing the molecular basis for apoC-II biosynthesis. cDNA cloning, nucleotide sequencing, and Northern blot mRNA quantification Nucleic acids research High 6328445
1985 ApoC-II (along with apoC-I and apoC-III isoforms) inhibits the uptake of triglyceride-rich lipoproteins and their remnants by the perfused rat liver; this inhibition is independent of apoE and applies to both chylomicron remnants and VLDL remnants. Preferential loss of apoC-II during remnant formation may regulate termination of triglyceride hydrolysis. Isolated perfused rat liver assay with exogenous addition of individual human C apolipoproteins to chylomicrons and VLDL remnants Journal of lipid research High 4020294
1991 ApoC-II inhibits apoE-dependent cellular uptake and degradation of triglyceride-rich lipoproteins via the LDL receptor pathway; the apoE:apoC ratio on the lipoprotein surface determines the extent of receptor-mediated uptake. ApoC-II does not affect LDL (apoB-100-mediated) metabolism significantly, demonstrating specificity for the apoE-dependent interaction. Cultured human skin fibroblast uptake/degradation assays using VLDL and IDL with exogenous recombinant apoE-3 and individual apoC species; monoclonal antibody blocking of apoB-100 vs. apoE The Journal of biological chemistry High 1917954
2001 Farnesoid X receptor (FXR) directly induces APOC2 transcription by binding two FXR response elements within hepatic control regions (HCR-1 and HCR-2) located 11 kb and 22 kb upstream of the apoC-II transcription start site; FXR/RXR heterodimers bind these elements by EMSA, and luciferase reporter assays confirm transactivation. In vivo, hepatic apoC-II mRNA increases in mice fed cholic acid (an FXR ligand), and this induction is absent in FXR-null mice, linking bile acid signaling to plasma triglyceride lowering via apoC-II. Suppression subtractive hybridization, retroviral FXR expression in HepG2 cells, EMSA with recombinant FXR/RXR, luciferase reporter assays, mouse dietary cholic acid feeding, FXR knockout mice Molecular endocrinology (Baltimore, Md.) High 11579204
2001 ABCA1 mediates cholesterol and phospholipid efflux using apoC-II (as well as apoA-I, apoA-II, apoA-IV, apoC-I, apoC-III, apoE) as acceptors; apoC-II promotes greater than 3-fold increase in lipid efflux from ABCA1-expressing cells compared to controls, indicating apoC-II can serve as a lipid acceptor for ABCA1-mediated reverse cholesterol transport. Stable transfection of ABCA1-GFP in HeLa cells, cholesterol and phospholipid efflux assays, specific binding assays Biochemical and biophysical research communications Medium 11162594
2001 ApoC-II forms amyloid fibers in lipid-free solutions under physiological conditions; macromolecular crowding (inert polymer dextran T10) significantly accelerates amyloid formation rate and extent via nonspecific volume exclusion, without altering secondary structure, fiber morphology, or dye-binding capacity of the fibers. Solution turbidity, thioflavin T reactivity, sedimentation assays, analytical ultracentrifugation, secondary structure analysis; quantitative modeling of volume exclusion The Journal of biological chemistry High 11751863
2002 The APOE/C-I/C-IV/C-II gene cluster is transcriptionally regulated by liver X receptors (LXRα/β) in macrophages; LXR/RXR ligands induce apoC-II mRNA 2–14-fold, this induction requires the LXR response elements in multienhancers ME.1 and ME.2 of the apoC-II promoter-reporter, and is abolished in LXRα/β double-null macrophages. ApoC-II protein co-localizes with macrophages within murine arterial lesions. Microarray, Northern blot, LXRα/β knockout murine macrophages, luciferase reporter assays with ME.1/ME.2 enhancer elements, immunohistochemistry of atherosclerotic lesions The Journal of biological chemistry High 12032151
2017 APOC2 knockout zebrafish (apoc2−/−) exhibit deficient plasma cholesterol esterification: significantly elevated free cholesterol to cholesterol ester ratio (FC/CE) compared to wild type, accompanied by dramatically decreased hepatic LCAT expression and apoA-I expression. This defect persists on low-fat diet even when triglycerides normalize, and is recapitulated in human FCS patients with APOC2 or LPL deficiency, revealing a novel link between LPL cofactor activity and LCAT-mediated cholesterol esterification. apoc2 knockout zebrafish, plasma FC/CE measurements, in situ hybridization, qPCR of lcat and apoA-I, LCAT activity assay in human FCS patient plasma, lipidomics of chylomicron-depleted fractions PloS one High 28107429
2020 ApoC2 is an obligatory activator of LPL for plasma triglyceride hydrolysis; CRISPR/Cas9 deletion of Apoc2 in golden Syrian hamsters causes severe hypertriglyceridemia that cannot be corrected by lipid-lowering medications but is fully reversed by AAV-hApoC2 gene therapy, demonstrating that ApoC2 is essential and sufficient for LPL-mediated triglyceride metabolism in a mammalian model. CRISPR/Cas9 Apoc2 knockout hamster, AAV-hApoC2 gene therapy rescue, lipid profile measurements, diet intervention, neonatal serum infusion rescue Metabolism: clinical and experimental High 32562799
2020 miR-1275 directly targets the 3′ UTR of ApoC2 mRNA in macrophages, suppressing ApoC2 protein expression; ApoC2 knockdown inhibits macrophage foam cell formation by reducing ox-LDL uptake, and ApoC2 overexpression promotes foam cell formation, placing ApoC2 downstream of miR-1275 in macrophage lipid accumulation relevant to ischemic stroke pathogenesis. Dual-luciferase reporter assay, miRNA microarray, quantitative RT-PCR, THP-1 macrophage foam cell assay with ox-LDL uptake measurement, siRNA knockdown Gene Medium 31935511
2020 miR-4510 directly targets APOC2 (confirmed by luciferase reporter assay); APOC2 knockdown in GIST cells suppresses cell proliferation, migration, and invasion, reduces AKT and ERK1/2 phosphorylation, and decreases MMP2/MMP9 expression, identifying APOC2 as a pro-tumorigenic factor acting through PI3K/AKT and MAPK/ERK signaling in gastrointestinal stromal tumors. Luciferase reporter assay, siRNA knockdown of APOC2, cell proliferation/migration/invasion assays, Western blotting for p-AKT, p-ERK1/2, MMP2, MMP9 Journal of cellular physiology Medium 31975384
2023 ApoC-II's C-terminal α-helix binds to regions of LPL surrounding the catalytic pocket (lid-anchoring structures), overlapping with the ANGPTL4 binding site on LPL. Unlike ANGPTL4, which destabilizes LPL's lid-anchoring regions and promotes irreversible unfolding, APOC2 binding increases LPL thermal stability and protects these regions from unfolding, providing a molecular mechanism for APOC2-mediated LPL activation through conformational stabilization of the active site. Hydrogen-deuterium exchange mass spectrometry (HDX-MS) with thermal stability assays comparing APOC2 vs. ANGPTL4 binding to LPL Proceedings of the National Academy of Sciences of the United States of America High 37094117
2022 APOC2 expression level defines distinct alveolar macrophage superclusters (families) in human bronchoalveolar lavage; differential APOC2/IFI27 expression distinguishes four AM supercluster identities, each containing functionally specialized subclusters, indicating APOC2 marks a transcriptionally and functionally distinct state in resident lung macrophages. Single-cell RNA sequencing of 113,213 bronchoalveolar lavage cells, TotalSeq protein surface marker validation, projection of external AM datasets Life science alliance Low 35820705
2022 In bovine adipocytes, miR-107 directly targets APOC2 (confirmed by luciferase reporter assay); APOC2 knockdown (siRNA) suppresses adipocyte differentiation and lipid droplet accumulation, while miR-107 overexpression (which reduces APOC2) similarly inhibits adipogenesis, establishing APOC2 as a positive regulator of bovine adipocyte differentiation and lipogenesis downstream of miR-107. Luciferase reporter assay, agomiR/antiagomiR transfection, siRNA-APOC2 knockdown, Oil Red O staining, CCK-8, EdU proliferation assay, RT-qPCR, Western blotting Genes Medium 36011378
2025 FXR activation upregulates ApoC2 expression in beige adipocytes (but not mature white adipocytes); ApoC2 overexpression in preadipocytes and beige adipocytes increases UCP1 and PGC1α expression, while FXR knockdown reduces ApoC2 along with UCP1, PGC1α, and PRDM16, placing ApoC2 downstream of FXR in a pathway promoting white adipose tissue browning and thermogenesis. FXR agonist (farnesol) treatment, siRNA knockdown of FXR and RXRα, ApoC2 overexpression in preadipocytes and beige adipocytes, Western blotting and RT-qPCR for beige/thermogenic markers, cold-exposure mouse model The Journal of biological chemistry Medium 39798876
2025 APOC2 knockdown in clear cell renal cell carcinoma (ccRCC) cell lines suppresses proliferation, colony formation, migration, and invasion while promoting apoptosis; silencing APOC2 reduces phosphorylation of JAK1/2 and STAT3 without affecting total protein levels, and the STAT3 agonist Colivelin partially rescues viability and apoptosis caused by APOC2 knockdown, indicating APOC2 promotes ccRCC progression at least partly through JAK-STAT pathway activation. siRNA knockdown of APOC2 in ccRCC cell lines, proliferation/colony/migration/invasion/apoptosis assays, Western blotting for p-JAK1/2 and p-STAT3, functional rescue with Colivelin (STAT3 agonist), gene set enrichment analysis Current issues in molecular biology Medium 41296440

Source papers

Stage 0 corpus · 64 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2010 Biological, clinical and population relevance of 95 loci for blood lipids. Nature 2873 20686565
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2008 Six new loci associated with blood low-density lipoprotein cholesterol, high-density lipoprotein cholesterol or triglycerides in humans. Nature genetics 1130 18193044
2008 Common variants at 30 loci contribute to polygenic dyslipidemia. Nature genetics 1113 19060906
2020 A reference map of the human binary protein interactome. Nature 849 32296183
1999 Patterns of single-nucleotide polymorphisms in candidate genes for blood-pressure homeostasis. Nature genetics 769 10391210
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2004 The human plasma proteome: a nonredundant list developed by combination of four separate sources. Molecular & cellular proteomics : MCP 658 14718574
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2006 Functionally defective high-density lipoprotein: a new therapeutic target at the crossroads of dyslipidemia, inflammation, and atherosclerosis. Pharmacological reviews 579 16968945
1973 Interchange of apolipoproteins between chylomicrons and high density lipoproteins during alimentary lipemia in man. The Journal of clinical investigation 514 4345202
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2012 Genome-wide association study identifies multiple loci influencing human serum metabolite levels. Nature genetics 436 22286219
2016 Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing. Cell 423 26871637
2010 Common inherited variation in mitochondrial genes is not enriched for associations with type 2 diabetes or related glycemic traits. PLoS genetics 363 20714348
2010 Genetic variants influencing circulating lipid levels and risk of coronary artery disease. Arteriosclerosis, thrombosis, and vascular biology 351 20864672
2001 Insight into hepatocellular carcinogenesis at transcriptome level by comparing gene expression profiles of hepatocellular carcinoma with those of corresponding noncancerous liver. Proceedings of the National Academy of Sciences of the United States of America 300 11752456
2001 Farnesoid X-activated receptor induces apolipoprotein C-II transcription: a molecular mechanism linking plasma triglyceride levels to bile acids. Molecular endocrinology (Baltimore, Md.) 283 11579204
1985 Inhibitory effects of C apolipoproteins from rats and humans on the uptake of triglyceride-rich lipoproteins and their remnants by the perfused rat liver. Journal of lipid research 278 4020294
2001 Apolipoprotein specificity for lipid efflux by the human ABCAI transporter. Biochemical and biophysical research communications 269 11162594
2004 An investigation into the human serum "interactome". Electrophoresis 247 15174051
2001 Macromolecular crowding accelerates amyloid formation by human apolipoprotein C-II. The Journal of biological chemistry 227 11751863
1991 Mechanisms of inhibition by apolipoprotein C of apolipoprotein E-dependent cellular metabolism of human triglyceride-rich lipoproteins through the low density lipoprotein receptor pathway. The Journal of biological chemistry 223 1917954
2012 Mutations in LPL, APOC2, APOA5, GPIHBP1 and LMF1 in patients with severe hypertriglyceridaemia. Journal of internal medicine 201 22239554
2002 Regulated expression of the apolipoprotein E/C-I/C-IV/C-II gene cluster in murine and human macrophages. A critical role for nuclear liver X receptors alpha and beta. The Journal of biological chemistry 198 12032151
1977 Primary structure of very low density apolipoprotein C-II of human plasma. Proceedings of the National Academy of Sciences of the United States of America 166 194244
2009 Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip. American journal of human genetics 164 19913121
1977 Activation of lipoprotein lipase by native and synthetic fragments of human plasma apolipoprotein C-II. Proceedings of the National Academy of Sciences of the United States of America 164 270715
1976 Effect of serum and C-apoproteins from very low density lipoproteins on human postheparin plasma hepatic lipase. FEBS letters 162 182536
2006 Isolation and characterization of human apolipoprotein M-containing lipoproteins. Journal of lipid research 161 16682745
1984 Human apolipoproteins AI, AII, CII and CIII. cDNA sequences and mRNA abundance. Nucleic acids research 136 6328445
1994 The putative glioma tumor suppressor gene on chromosome 19q maps between APOC2 and HRC. Cancer research 81 8062276
1988 Apolipoprotein gene cluster on chromosome 19. Definite localization of the APOC2 gene and the polymorphic Hpa I site associated with type III hyperlipoproteinemia. Human genetics 68 2892779
2018 DNA methylation of TOMM40-APOE-APOC2 in Alzheimer's disease. Journal of human genetics 66 29371683
2022 ScRNA-seq expression of IFI27 and APOC2 identifies four alveolar macrophage superclusters in healthy BALF. Life science alliance 51 35820705
2017 A Novel APOC2 Missense Mutation Causing Apolipoprotein C-II Deficiency With Severe Triglyceridemia and Pancreatitis. The Journal of clinical endocrinology and metabolism 33 28201738
2020 ApoC2 deficiency elicits severe hypertriglyceridemia and spontaneous atherosclerosis: A rodent model rescued from neonatal death. Metabolism: clinical and experimental 30 32562799
1991 The human chromosome 19 linkage group FUT1 (H), FUT2 (SE), LE, LU, PEPD, C3, APOC2, D19S7 and D19S9. Annals of human genetics 29 1763885
2007 Preimplantation genetic diagnosis for myotonic dystrophy type 1: detection of crossover between the gene and the linked marker APOC2. Prenatal diagnosis 23 17192963
2016 A novel APOC2 gene mutation identified in a Chinese patient with severe hypertriglyceridemia and recurrent pancreatitis. Lipids in health and disease 21 26772541
1988 The chromosome 19 linkage group LDLR, C3, LW, APOC2, LU, SE in man. Annals of human genetics 20 2907851
1989 Recombination events that locate myotonic dystrophy distal to APOC2 on 19q. Genomics 19 2591962
2023 Inverse effects of APOC2 and ANGPTL4 on the conformational dynamics of lid-anchoring structures in lipoprotein lipase. Proceedings of the National Academy of Sciences of the United States of America 18 37094117
2014 Apolipoprotein C-II Tuzla: a novel large deletion in APOC2 caused by Alu-Alu homologous recombination in an infant with apolipoprotein C-II deficiency. Clinica chimica acta; international journal of clinical chemistry 16 25172036
2020 miR-4510 acts as a tumor suppressor in gastrointestinal stromal tumor by targeting APOC2. Journal of cellular physiology 14 31975384
1993 Genetic variation of microsatellite markers D1S117, D6S89, D11S35, APOC2, and D21S168 in the Spanish population. International journal of legal medicine 13 8471544
2020 AAV-Mediated ApoC2 Gene Therapy: Reversal of Severe Hypertriglyceridemia and Rescue of Neonatal Death in ApoC2-Deficient Hamsters. Molecular therapy. Methods & clinical development 12 32802915
2017 Deficient Cholesterol Esterification in Plasma of apoc2 Knockout Zebrafish and Familial Chylomicronemia Patients. PloS one 10 28107429
1994 Genetic studies on the Senegal population. II. Polymorphisms of the plasma proteins F13A, F13B, ORM1, AHSG, C6, C7, and APOC2. Human biology 10 8001915
1988 Segregation of linked probes to myotonic dystrophy in a family demonstrating that 152 and APOC2 are on the same side of DM on 19q. Human genetics 8 3198115
2020 Blood miR-1275 is associated with risk of ischemic stroke and inhibits macrophage foam cell formation by targeting ApoC2 gene. Gene 7 31935511
2024 Pancreatitis as a Main Consequence of APOC2-Related Hypertriglyceridemia: The Role of Nonsense and Frameshift Variants. International journal of genomics 6 38938447
2023 Comprehensive in-silico analysis of deleterious SNPs in APOC2 and APOA5 and their differential expression in cancer and cardiovascular diseases conditions. Genomics 6 36690263
2022 MiR-107 Regulates Adipocyte Differentiation and Adipogenesis by Targeting Apolipoprotein C-2 (APOC2) in Bovine. Genes 6 36011378
2020 A Novel APOC2 Mutation in a Colombian Patient with Recurrent Hypertriglyceridemic Pancreatitis. The application of clinical genetics 6 32280258
2020 Experimental Therapeutics for Challenging Clinical Care of a Patient with an Extremely Rare Homozygous APOC2 Mutation. Case reports in endocrinology 6 32292609
2020 Sequence analysis of the coding regions of the apolipoprotein C2 (APOC2) gene in Miniature Schnauzers with idiopathic hypertriglyceridemia. Veterinary journal (London, England : 1997) 6 33129550
2013 Apolipoprotein C-II deficiency with no rare variant in the APOC2 gene. Journal of atherosclerosis and thrombosis 6 23470567
1988 Presymptomatic testing for myotonic dystrophy by means of the linked DNA marker APOC2. The Medical journal of Australia 5 3047535
2025 FXR-ApoC2 pathway activates UCP1-mediated thermogenesis by promoting the browning of white adipose tissues. The Journal of biological chemistry 4 39798876
2018 Severe hyperchylomicronemia in two infants with novel APOC2 gene mutation. Journal of pediatric endocrinology & metabolism : JPEM 4 30307897
2010 Identification of mutations in the lipoprotein lipase (LPL) and apolipoprotein C-II (APOC2) genes using denaturing high performance liquid chromatography (DHPLC). Clinica chimica acta; international journal of clinical chemistry 2 20940006
2025 High-throughput screening reveals paeoniflorin's efficacy against Apoc2-deficient hypertriglyceridemia via HNF4A/PPARA/LDLR. Biochemical pharmacology 1 40983153
2025 APOC2 Promotes Clear Cell Renal Cell Carcinoma Progression via Activation of the JAK-STAT Signaling Pathway. Current issues in molecular biology 0 41296440