Contact Us

The choice depends on whether you are studying ACOT8 (acyl-CoA thioesterase 8)'s role as a peroxisomal acyl-CoA thioesterase or modeling its functions in lipid metabolism. The Knockout line is the standard tool for asking whether ACOT8 is required for these processes — ACOT8 is a peroxisomal thioesterase that hydrolyzes acyl-CoA esters (including medium/long-chain, bile acid-CoA, and others) to free fatty acid and CoA, regulating intracellular acyl-CoA/CoA pools and peroxisomal fatty acid oxidation; ACOT8 also has a reported interaction with HIV-1 Nef. Overexpression is useful for studying ACOT8 gain-of-function effects. For peroxisomal lipid metabolism research, the EDITGENE ACOT8 Knockout in HeLa enables study of ACOT8 biology. Other ACOT family members expression analysis aids interpretation. Rescue with wild-type or catalytically-dead ACOT8 enables structure-function studies. The knockout is valuable for studying peroxisomal acyl-CoA thioesterase biology, CoA homeostasis, and peroxisomal fatty acid oxidation regulation.

Yes. ACOT8 rescue experiments require attention to peroxisomal targeting: • Construct design: use a codon-modified ACOT8 sequence with a small N-terminal tag (FLAG, HA) — ACOT8 has a C-terminal PTS1 peroxisomal targeting signal that must be preserved for proper localization; C-terminal tags may disrupt peroxisomal import. • Peroxisomal localization validation: confirm peroxisomal localization before functional assays. • Catalytically-dead rescue: active site Ser/Asp/His catalytic triad mutations abolish thioesterase activity. • Functional readout: rescue should restore peroxisomal acyl-CoA thioesterase activity. HeLa transduces efficiently with lentivirus and supports stable rescue line generation.

The choice depends on the experimental question. ACSBG2 (acyl-CoA synthetase bubblegum family member 2) is a less-characterized long-chain/very-long-chain acyl-CoA synthetase. The Knockout line is appropriate for asking whether ACSBG2 is required for predicted activities — ACSBG2 is a member of the 'bubblegum' acyl-CoA synthetase family (ACSBG1, ACSBG2) that activates long-chain and very-long-chain fatty acids; ACSBG2 is expressed in testis and brain with roles in fatty acid activation, and has reported functions in steroidogenesis. Overexpression is useful for studying ACSBG2 in heterologous expression contexts. For fatty acid metabolism research, the EDITGENE ACSBG2 Knockout in HeLa provides a clean genetic background for characterizing ACSBG2-specific functions. ACSBG1 paralog expression analysis aids interpretation. Rescue with wild-type or catalytically-dead ACSBG2 is the standard specificity control. The knockout is valuable for studying bubblegum family acyl-CoA synthetase biology and emerging ACSBG2 functions.

Yes. ACSBG2 rescue experiments require attention to bubblegum family architecture: • Construct design: use a codon-modified ACSBG2 sequence with a small C-terminal tag (FLAG, HA). ACSBG2 has the bubblegum acyl-CoA synthetase architecture — preserve protein integrity. • Catalytically-dead rescue: ATP-binding region mutations abolish acyl-CoA synthetase activity. • Functional readout: rescue should restore long/very-long-chain acyl-CoA synthesis. HeLa transduces efficiently with lentivirus and supports stable rescue line generation.

The choice depends on whether you are studying APOE's role as a major lipoprotein component or modeling APOE genotype effects in cardiovascular and Alzheimer's disease. The Knockout line is the standard tool for asking whether APOE is required for these processes — APOE is a 299-aa secreted lipoprotein component principally synthesized in liver (also brain astrocytes/microglia) that binds LDL receptor family (LDLR, LRP1) for lipoprotein clearance; APOE has three major isoforms (ε2, ε3, ε4) defined by cysteine/arginine at residues 112 and 158 — ⭐⭐⭐ APOE4 (R112, R158) is the single strongest genetic risk factor for late-onset Alzheimer's disease, while APOE2 is protective. Overexpression is useful for studying APOE isoform effects. For lipoprotein metabolism and AD research, the EDITGENE APOE Knockout in Hep-G2 is uniquely valuable — Hep-G2 is a hepatocellular carcinoma line, providing the principal context for hepatic APOE synthesis (the main source of plasma APOE). Rescue with APOE2 (C112, C158), APOE3 (C112, R158), or APOE4 (R112, R158) enables isoform-specific functional dissection — gold-standard experimental design for studying APOE allelic variation. The knockout is valuable for studying hepatic lipoprotein assembly, APOE4-driven AD risk mechanisms, and emerging APOE-targeted therapeutics (APOE-mimetic peptides, anti-APOE antibodies).

Yes, and rescue experiments are uniquely powerful for APOE isoform research: • Construct design: use codon-modified APOE2, APOE3, or APOE4 sequences with small C-terminal tags (FLAG, HA, after signal peptide cleavage). APOE has signal peptide, N-terminal receptor-binding domain (LDL receptor binding), and C-terminal lipid-binding domain — preserve all elements. • Isoform-specific rescue: ⭐⭐⭐ APOE2 (C112, C158), APOE3 (C112, R158), APOE4 (R112, R158) — gold-standard experimental design for APOE genetic variation research. • Receptor-binding-deficient rescue: R142C or R145A mutations in receptor-binding region disrupt LDLR binding. • Secretion validation: confirm conditioned media APOE secretion by ELISA. • Functional readout: rescue should restore lipoprotein assembly and LDLR-mediated clearance. Hep-G2 transduces efficiently with lentivirus and supports stable rescue line generation.

The choice depends on whether you are studying AKAP11 (A-kinase anchor protein 11, AKAP220)'s role as a PKA scaffold and GSK3β-binding protein or modeling its breakthrough role as a bipolar disorder/schizophrenia shared risk gene. The Knockout line is the standard tool for asking whether AKAP11 is required for these processes — AKAP11 is an A-kinase anchor protein that scaffolds protein kinase A (PKA) at specific subcellular locations, and importantly binds GSK3β — the hypothesized molecular target of lithium (the principal treatment for bipolar disorder). Overexpression is useful for studying AKAP11 in heterologous expression contexts. For psychiatric disease research, the EDITGENE AKAP11 Knockout in HAP1 is a uniquely valuable tool — landmark exome sequencing studies (Palmer et al. Nature Genetics 2022) identified ⭐⭐ AKAP11 as a definitive shared risk gene for both bipolar disorder and schizophrenia, with ultra-rare protein-truncating variants conferring OR = 7.06 (P = 2.83 × 10⁻⁹) — one of the largest effect-size psychiatric risk genes; subsequent Nature Genetics 2025 (Iceland + UK Biobank) confirmed AKAP11 plus HECTD2 in bipolar disorder. Rescue with wild-type or PTV (protein-truncating) AKAP11 enables disease modeling; ⭐ GSK3β-binding-deficient rescue separates AKAP11's PKA scaffolding from GSK3β interaction. The knockout is uniquely valuable for studying psychiatric disease mechanisms, lithium pharmacology, and emerging GSK3β-axis psychiatric therapeutics — this is one of the most important recent discoveries in psychiatric genetics.

Yes. AKAP11 rescue experiments are uniquely valuable for psychiatric disease research: • Construct design: use a codon-modified AKAP11 sequence with a small C-terminal tag (FLAG, HA). AKAP11 is a ~210 kDa scaffold protein with PKA-binding amphipathic helix and GSK3β-binding region — preserve all elements. • Bipolar disorder/schizophrenia mutation rescue: ⭐ patient-derived protein-truncating variants (PTVs) from the BipEx and SCHEMA studies enable disease genotype-function studies. • GSK3β-binding-deficient rescue: rescue with GSK3β-binding-region mutations separates PKA scaffolding from GSK3β interaction — uniquely useful for studying the proposed lithium-AKAP11-GSK3β axis. • PKA-binding-deficient rescue: amphipathic helix mutations disrupt PKA scaffolding. • Functional readout: rescue should restore PKA subcellular localization and GSK3β interaction. HAP1-specific considerations: • Diploidization: HAP1 cells gradually diploidize during extended culture — confirm ploidy by flow cytometry at the time of phenotypic assay. • Integration site sensitivity: position effects on transgene expression are more pronounced in near-haploid backgrounds; generating multiple independent rescue clones is strongly recommended. • Transduction efficiency: HAP1 transduces with lentivirus at moderate efficiency — increase MOI compared to standard immortalized lines.

The choice depends on whether you are studying ACSL3 (long-chain acyl-CoA synthetase 3)'s role in lipid metabolism or modeling its functions in ferroptosis, lipid droplets, and emerging cancer applications. The Knockout line is the standard tool for asking whether ACSL3 is required for these processes — ACSL3 is a long-chain fatty acyl-CoA synthetase that activates fatty acids (especially monounsaturated and some polyunsaturated FAs) to acyl-CoA for lipid synthesis and lipid droplet formation; ACSL3 has emerging roles as a protective factor against ferroptosis (in contrast to ACSL4, which promotes ferroptosis by enriching PUFAs in membranes) and in viral replication (used by multiple viruses for lipid droplet biogenesis). Overexpression is useful for studying ACSL3 gain-of-function effects. For lipid metabolism and ferroptosis research, the EDITGENE ACSL3 Knockout in HAP1 enables study of ACSL3 biology. Other ACSL family members (ACSL1, ACSL4, ACSL5, ACSL6) expression analysis aids interpretation; the ACSL3/ACSL4 balance is particularly important in ferroptosis. Rescue with wild-type or catalytically-dead ACSL3 enables structure-function studies. The knockout is valuable for studying lipid droplet biology, ferroptosis sensitivity (ACSL3 promotes MUFA incorporation that protects against ferroptosis), and emerging ACSL3-related cancer metabolism.

Yes. ACSL3 rescue experiments require attention to acyl-CoA synthetase architecture: • Construct design: use a codon-modified ACSL3 sequence with a small C-terminal tag (FLAG, HA). ACSL3 has N-terminal membrane anchor, central ATP/AMP-binding region, and fatty acid-binding region — preserve all elements. • Catalytically-dead rescue: ATP-binding region mutations abolish acyl-CoA synthetase activity. • Functional readout: rescue should restore long-chain acyl-CoA synthesis and ferroptosis-protective MUFA incorporation. HAP1-specific considerations: • Diploidization: HAP1 cells gradually diploidize during extended culture — confirm ploidy by flow cytometry at the time of phenotypic assay. • Integration site sensitivity: position effects on transgene expression are more pronounced in near-haploid backgrounds; generating multiple independent rescue clones is strongly recommended. • Transduction efficiency: HAP1 transduces with lentivirus at moderate efficiency — increase MOI compared to standard immortalized lines.

The choice depends on the experimental question. AATK (apoptosis-associated tyrosine kinase, LMTK1) is a less-characterized membrane-anchored kinase. The Knockout line is appropriate for asking whether AATK is required for predicted activities — AATK (also called LMTK1, lemur tyrosine kinase 1) is a transmembrane Ser/Thr kinase (despite the 'tyrosine kinase' name) of the LMTK family (LMTK1/AATK, LMTK2, LMTK3) with characterized roles in neuronal differentiation, endosomal trafficking (Rab11 regulation), and apoptosis. Overexpression is useful for studying AATK in heterologous expression contexts. Important nomenclature note: despite 'tyrosine kinase' in the name, AATK/LMTK1 functions predominantly as a serine/threonine kinase. For LMTK family research, the EDITGENE AATK Knockout in HAP1 provides a clean genetic background for characterizing AATK-specific functions. LMTK2, LMTK3 paralog expression analysis aids interpretation. Rescue with wild-type or kinase-dead AATK is the standard specificity control. The knockout is valuable for studying LMTK family biology, neuronal differentiation, and endosomal recycling. HAP1-specific considerations: • Diploidization: HAP1 cells gradually diploidize during extended culture — confirm ploidy by flow cytometry at the time of phenotypic assay. • Integration site sensitivity: position effects on transgene expression are more pronounced in near-haploid backgrounds; generating multiple independent rescue clones is strongly recommended. • Transduction efficiency: HAP1 transduces with lentivirus at moderate efficiency — increase MOI compared to standard immortalized lines.

Yes. AATK rescue experiments require attention to membrane-anchored kinase architecture: • Construct design: use a codon-modified AATK sequence with a small C-terminal tag (FLAG, HA). AATK has N-terminal transmembrane domain, kinase domain, and long C-terminal regulatory tail — preserve membrane anchoring. • Kinase-dead rescue: ATP-binding lysine mutation abolishes catalytic activity (note: AATK functions as a Ser/Thr kinase despite its name). • Functional readout: rescue should restore AATK-dependent endosomal recycling and substrate phosphorylation. HAP1-specific considerations: • Diploidization: HAP1 cells gradually diploidize during extended culture — confirm ploidy by flow cytometry at the time of phenotypic assay. • Integration site sensitivity: position effects on transgene expression are more pronounced in near-haploid backgrounds; generating multiple independent rescue clones is strongly recommended. • Transduction efficiency: HAP1 transduces with lentivirus at moderate efficiency — increase MOI compared to standard immortalized lines.

The choice depends on whether you are studying ABCA1 (ATP-binding cassette transporter A1)'s role as the principal cholesterol efflux transporter or modeling Tangier disease and cardiovascular biology. The Knockout line is the standard tool for asking whether ABCA1 is required for these processes — ABCA1 is an ABC full-transporter that mediates the efflux of cellular cholesterol and phospholipids to lipid-poor apolipoprotein A-I (apoA-I), the rate-limiting first step of reverse cholesterol transport and HDL biogenesis; ABCA1 is critical for cellular cholesterol homeostasis. Overexpression is useful for studying ABCA1 gain-of-function effects. For lipid metabolism and cardiovascular research, the EDITGENE ABCA1 Knockout in HAP1 is uniquely valuable — ABCA1 biallelic loss-of-function causes ⭐⭐ Tangier disease (severe HDL deficiency, cholesterol ester accumulation in tissues, enlarged orange tonsils, premature atherosclerosis); heterozygous ABCA1 mutations cause familial hypoalphalipoproteinemia. Rescue with wild-type or patient-derived ABCA1 mutations enables disease modeling. The knockout is valuable for studying reverse cholesterol transport, HDL biogenesis, macrophage cholesterol efflux (atherosclerosis), and emerging ABCA1-modulating cardiovascular therapeutics (LXR agonists upregulate ABCA1). HAP1-specific considerations: • Diploidization: HAP1 cells gradually diploidize during extended culture — confirm ploidy by flow cytometry at the time of phenotypic assay. • Integration site sensitivity: position effects on transgene expression are more pronounced in near-haploid backgrounds; generating multiple independent rescue clones is strongly recommended. • Transduction efficiency: HAP1 transduces with lentivirus at moderate efficiency — increase MOI compared to standard immortalized lines.

Yes. ABCA1 rescue experiments are well-established for cholesterol efflux research: • Construct design: use a codon-modified ABCA1 sequence with a small intracellular tag (FLAG, HA). ABCA1 is a full ABC transporter with two transmembrane domains, two large extracellular loops, and two nucleotide-binding domains — preserve membrane topology. • Surface localization validation: confirm plasma membrane localization before cholesterol efflux assays. • Transport-deficient rescue: Walker A motif mutations abolish ATP-dependent lipid efflux. • Tangier disease mutation rescue: patient-derived ABCA1 mutations enable disease modeling. • Functional readout: rescue should restore apoA-I-mediated cholesterol efflux. HAP1-specific considerations: • Diploidization: HAP1 cells gradually diploidize during extended culture — confirm ploidy by flow cytometry at the time of phenotypic assay. • Integration site sensitivity: position effects on transgene expression are more pronounced in near-haploid backgrounds; generating multiple independent rescue clones is strongly recommended. • Transduction efficiency: HAP1 transduces with lentivirus at moderate efficiency — increase MOI compared to standard immortalized lines.

The choice depends on whether you are studying APOD (apolipoprotein D)'s role as a lipocalin family secreted protein or modeling its functions in neurodegeneration and emerging biology. The Knockout line is the standard tool for asking whether APOD is required for these processes — APOD is an atypical apolipoprotein belonging to the lipocalin family (unlike other apolipoproteins which are amphipathic helix-rich); APOD has a typical lipocalin β-barrel that binds hydrophobic ligands (progesterone, pregnenolone, arachidonic acid, possibly oxidized lipids); APOD is highly expressed in nervous system and is a major component of breast cyst fluid. Overexpression is useful for studying APOD gain-of-function effects. For APOD research, the EDITGENE APOD Knockout in HEK293T is a workhorse mechanistic platform. This product complements the parallel APOD Knockout in A-549 (also available) for cross-background validation. Rescue with wild-type APOD is the standard specificity control. The knockout is valuable for studying lipocalin family biology, neuroprotection mechanisms (APOD upregulation in aging and neurodegeneration), and emerging APOD-related biology.