Contact Us

Yes, and rescue experiments are uniquely powerful in this double knockout: • Single-isoform rescue: re-introduction of DTWD1 alone or DTWD2 alone in the double knockout enables position-specific functional dissection (DTWD1 modifies position 20; DTWD2 modifies position 20a) — gold-standard experimental design for paralog dissection. • Construct design: use codon-modified DTWD1 or DTWD2 sequences with small C-terminal tags (FLAG, HA). Preserve DTW domain integrity in each paralog. • Catalytically-dead rescue: active site mutations enable separation of catalytic from structural functions. • Functional readout: rescue should restore position-specific acp³U levels and reverse the growth retardation phenotype reported in double knockout cells. HEK293 transduces efficiently with lentivirus and supports systematic isoform-specific rescue experiments.

The choice depends on whether you are studying combined DTWD1/DTWD2 function or distinguishing complete acp³U-deficient phenotypes. The Double Knockout line is uniquely valuable for asking whether DTWD1/DTWD2 are required for global acp³U tRNA modification — DTWD1 and DTWD2 catalyze acp³U at different tRNA positions (DTWD1 at position 20, DTWD2 at position 20a); combined loss eliminates acp³U at both positions, generating completely acp³U-deficient tRNAs. Single-isoform rescue (DTWD1 alone or DTWD2 alone) in the double knockout enables position-specific functional dissection. For tRNA modification research, the EDITGENE DTWD1 & DTWD2 Double Knockout in HEK293 is the gold-standard genetic tool — Takakura et al. (Nature Communications 2019) reported that DTWD1+DTWD2 double knockout cells exhibit growth retardation, indicating that acp³U is physiologically important in mammals. Single-isoform rescue is the gold-standard experimental design for paralog dissection. The double knockout is uniquely valuable for studying acp³U-dependent tRNA biology, translation fidelity, and emerging tRNA modification-related disease research.

Yes. TLR7/8 rescue experiments are uniquely valuable in this double knockout background: • Single-receptor rescue: re-introduction of TLR7 alone or TLR8 alone in the double knockout background is the gold-standard experimental design for distinguishing receptor-specific functions, since the two receptors are functionally redundant for many ssRNA ligands. • Construct design: use codon-modified TLR7 or TLR8 sequences with C-terminal tags. Both are type I membrane proteins with endosomal localization — N-terminal signal peptides must be preserved. • Endosomal localization validation: confirm endosomal compartment localization by immunofluorescence (LAMP1, Rab9 co-staining) before functional assays. • Agonist selectivity studies: TLR7-selective agonists (gardiquimod) versus TLR8-selective agonists (VTX-2337/motolimod) and dual agonists (R848) can be directly compared in single-rescue lines. THP-1 is a suspension cell line — transduction is typically performed via spinoculation with lentivirus; consider PMA-induced differentiation context for functional readouts.

The choice depends on whether you are studying ssRNA virus sensing, vaccine adjuvant mechanisms, or the redundancy and specialization between TLR7 and TLR8. The double Knockout line is appropriate for asking whether TLR7 and TLR8 are required jointly for these processes — single TLR7 or TLR8 knockouts often show mild phenotypes due to functional redundancy, which the double knockout eliminates. Overexpression is useful for testing receptor-specific ligand selectivity or for sufficiency studies. For TLR7/8 research, the EDITGENE Double Knockout in THP-1 is highly informative for vaccine adjuvant development (R848/resiquimod and related TLR7/8 agonists are clinical-stage adjuvants) and antiviral immunity studies — THP-1 is the standard human monocytic cell line for innate immune signaling research. Rescue with TLR7 alone or TLR8 alone enables direct dissection of receptor-specific contributions in a clean double-knockout background, which is the gold standard experimental design for distinguishing TLR7 and TLR8 functions.

Yes, and rescue experiments are uniquely powerful in this double knockout: • Single-isoform rescue: re-introduction of ESYT2 alone or ESYT3 alone in the double knockout enables paralog-specific functional dissection — gold-standard experimental design. • Construct design: use codon-modified ESYT2 or ESYT3 sequences with small C-terminal tags (FLAG, HA). Preserve ER hairpin, SMP domain, and C2 domain architecture. • SMP-domain or C2-domain mutant rescue: enables structure-function dissection within each paralog. • ESYT1 residual: rescue interpretation considers residual ESYT1 expression contributing to ER-PM contact sites. • Functional readout: rescue should restore ER-PM contact site lipid transfer activity. HEK293 transduces efficiently with lentivirus and supports systematic isoform-specific rescue experiments.

The choice depends on whether you are studying combined ESYT2/ESYT3 function or distinguishing ESYT2/ESYT3-dependent from ESYT1-dependent ER-PM contact site functions. The Double Knockout line is uniquely valuable for asking whether ESYT2/ESYT3 are required for these processes — ESYT2 and ESYT3 share substantial functional overlap as ER-PM contact site lipid transfer proteins; single knockouts retain residual activity from the other paralog, while double knockout eliminates ESYT2/ESYT3 functions, leaving only ESYT1. Single-isoform rescue (ESYT2 alone or ESYT3 alone) in the double knockout enables paralog-specific functional dissection. For ER-PM contact site research, the EDITGENE ESYT2 & ESYT3 Double Knockout in HEK293 is the gold-standard genetic tool — combined loss eliminates the most-characterized ESYT family members. Single-isoform rescue (ESYT2 alone or ESYT3 alone) is the gold-standard experimental design for paralog dissection. ESYT1 paralog expression analysis aids interpretation. The double knockout is uniquely valuable for studying glycerophospholipid transfer dynamics, PI(4,5)P2 replenishment at PM, and emerging ESYT family-targeted approaches.

Yes, and rescue experiments are uniquely powerful in this double knockout background: • Single-SNARE rescue: re-introduction of SNAP23 alone or STX7 alone enables dissection of independent functions — the gold-standard experimental design for partnered Q-SNARE biology. • Combined rescue: simultaneous SNAP23 + STX7 re-expression restores partnered fusion capacity and serves as the positive control. • Construct design: codon-modified SNAP23 and STX7 sequences with small tags (FLAG, HA). Both are essential for late endosomal/lysosomal fusion — preserve SNARE motifs and transmembrane anchoring. • Functional readout: late endosome-lysosome fusion assays, cathepsin maturation, and autophagic flux to confirm restoration of combined SNARE function. HEK293T's very high transfection efficiency enables combinatorial rescue experiments that would be difficult to execute in less efficient cell lines.

The choice depends on whether you are studying combined Q-SNARE function in endolysosomal fusion or distinguishing SNAP23's roles in different fusion compartments. The Double Knockout line is uniquely valuable for asking whether SNAP23 and STX7 function together — these SNAREs partner in late endosomal/lysosomal fusion events that single knockouts cannot fully reveal. Overexpression of either SNARE in the double knockout is useful for sufficiency testing and for rescue with SNARE variants. For endolysosomal SNARE research, the EDITGENE SNAP23 & STX7 Double Knockout in HEK293T is highly informative — STX7 is a late endosomal/lysosomal syntaxin that partners with SNAP23 in heterotypic membrane fusion. Single-SNARE rescue (SNAP23 alone or STX7 alone) in the double knockout dissects independent versus partnered functions. Rescue with both SNAREs restores combined fusion capacity. This combinatorial approach is the gold standard for studying compartment-specific SNARE biology.

Yes, and rescue experiments are uniquely powerful in this double knockout: • Single-isoform rescue: ⭐ re-introduction of ACVR2A alone or ACVR2B alone in the double knockout enables paralog-specific functional dissection — gold-standard experimental design for the type II activin receptor pair. • Construct design: use codon-modified ACVR2A or ACVR2B sequences with small intracellular C-terminal tags (FLAG, HA) — preserve extracellular ligand-binding domain, transmembrane span, and kinase domain. • Kinase-dead rescue: K219R (ACVR2A) or K217R (ACVR2B) ATP-binding lysine mutations abolish catalytic activity. • Ligand-binding-deficient rescue: extracellular domain mutations enable separation of ligand-trapping from signaling. • Functional readout: rescue should restore activin/myostatin/GDF11-induced phospho-SMAD2/3; paralog-specific rescue reveals ACVR2A vs ACVR2B distinct contributions. HEK293 transduces efficiently with lentivirus and supports systematic isoform-specific rescue experiments for activin/myostatin ligand-trap research.

ACVR2A and ACVR2B are the two type II activin receptors — serine/threonine kinase receptors that bind activins, myostatin (GDF8), GDF11, BMPs, and other TGF-β superfamily ligands; upon ligand binding, the type II receptor recruits and phosphorylates type I receptors (ALK4/ACVR1B, ALK5, ALK7), which then phosphorylate SMAD2/3 (activin/myostatin branch) to regulate gene expression. ACVR2A and ACVR2B share substantial ligand and functional overlap, with myostatin/GDF11-mediated muscle growth suppression being a major shared function. This ligand-trap axis is the basis of several clinically important therapeutics. This ACVR2A & ACVR2B Double Knockout in HEK293 is the gold-standard genetic tool for asking whether type II activin receptors are required for these processes — combined loss of ACVR2A and ACVR2B eliminates virtually all activin/myostatin/GDF11 type II receptor signaling, generating cells unable to transduce these TGF-β superfamily signals. Single-isoform rescue (ACVR2A alone or ACVR2B alone) in the double knockout enables paralog-specific functional dissection — the gold-standard experimental design for this receptor pair. For systematic activin/myostatin research, the EDITGENE ACVR2A & ACVR2B Double Knockout in HEK293 is uniquely valuable — single knockouts retain residual signaling from the other paralog; double knockout completely abolishes type II activin receptor function. This product complements the parallel single ACVR2A Knockouts in HEK293 and HAP1 (both also available). The double knockout is a critical specificity tool for ⭐⭐ sotatercept (Winrevair, FDA-approved 2024 for pulmonary arterial hypertension — a landmark PAH therapy), luspatercept (Reblozyl, for anemia), bimagrumab (anti-ActRII antibody for muscle wasting and obesity/metabolic disease), ramatercept, and the entire activin/myostatin ligand-trap therapeutic class — these traps act on both ACVR2A and ACVR2B, making the double knockout the definitive specificity control.

Yes, and rescue experiments are uniquely powerful in this double knockout for biased GPCR research: • Single-isoform rescue: re-introduction of ARRB1 alone or ARRB2 alone enables paralog-specific functional dissection — gold-standard experimental design for β-arrestin paralog biology. • Construct design: use codon-modified ARRB1 or ARRB2 sequences with small C-terminal tags (FLAG, HA) — small tags preserve β-arrestin conformational changes. • Phosphorylation-independent mutant rescue: R169E (β-arrestin 1) or analogous mutations generate phosphorylation-independent active β-arrestin for biased agonism research. • Functional readout: rescue should restore agonist-induced GPCR internalization and β-arrestin-mediated MAPK signaling. HEK293T transduces with very high efficiency and supports systematic isoform-specific rescue experiments.

The choice depends on whether you are studying combined β-arrestin 1/2 functions or modeling biased GPCR agonism. The Double Knockout line is the gold-standard tool for asking whether β-arrestins are required for GPCR functions — ARRB1 (β-arrestin 1) and ARRB2 (β-arrestin 2) are highly homologous scaffold proteins that bind agonist-occupied phosphorylated GPCRs, mediating receptor desensitization, internalization, and G-protein-independent signaling (ERK, p38, JNK activation through β-arrestin-MAPK scaffolding). Combined β-arrestin 1/2 double knockout eliminates β-arrestin-mediated signaling, enabling pure G-protein-only GPCR analysis. For GPCR pharmacology research, the EDITGENE ARRB1 & ARRB2 Double Knockout in HEK293T is the gold-standard genetic tool — HEK293T's very high transfection efficiency supports systematic biased agonism research. Single β-arrestin paralogs share substantial functional overlap — double knockout completely eliminates β-arrestin-mediated functions. Single-isoform rescue (ARRB1 alone or ARRB2 alone) enables paralog-specific functional dissection — gold-standard experimental design. The double knockout is uniquely valuable for studying ⭐⭐ biased GPCR agonism (G-protein-biased vs β-arrestin-biased ligands), GPCR-targeted drug development with biased activation profiles (TRV027 angiotensin biased, oliceridine/Olinvyk biased μ-opioid), and emerging biased GPCR therapeutics.

Yes, and rescue experiments are uniquely powerful in this double knockout: • Single-isoform rescue: ⭐ re-introduction of ALK4 (ACVR1B) alone or ALK5 (TGFBR1) alone enables receptor-specific dissection of activin vs TGF-β SMAD2/3 signaling — gold-standard experimental design. • Construct design: use codon-modified ACVR1B or TGFBR1 sequences with small intracellular C-terminal tags (FLAG, HA) — preserve extracellular, GS, and kinase domains. • Kinase-dead rescue: K234R (ALK4) or K232R (ALK5) ATP-binding lysine mutations abolish catalytic activity. • Constitutively active rescue: T206D (ALK4) or T204D (ALK5) GS domain mutations generate constitutively active receptors. • Functional readout: rescue should restore activin (ALK4) or TGF-β (ALK5)-induced phospho-SMAD2/3. HEK293 transduces efficiently with lentivirus and supports systematic isoform-specific rescue experiments.

The choice depends on whether you are studying combined activin (ALK4) and TGF-β (ALK5) type I receptor signaling or distinguishing their contributions to SMAD2/3 activation. The Double Knockout line is uniquely valuable for asking whether ALK4/ALK5 are required for SMAD2/3 signaling — ACVR1B/ALK4 (activin type I receptor) and TGFBR1/ALK5 (TGF-β type I receptor) are the two principal SMAD2/3-activating type I receptors; ALK4 transduces activin signals and ALK5 transduces TGF-β signals, but they share the SMAD2/3 effector branch. Combined ALK4/ALK5 knockout eliminates most SMAD2/3-activating signaling. Single-isoform rescue (ALK4 alone or ALK5 alone) enables receptor-specific dissection of activin versus TGF-β signaling. For SMAD2/3 signaling research, the EDITGENE ACVR1B & TGFBR1 Double Knockout in HEK293 is the gold-standard genetic tool for distinguishing activin from TGF-β signaling — single knockouts retain residual SMAD2/3 activation from the other receptor. Single-isoform rescue is the gold-standard experimental design. The double knockout is a critical specificity tool for ⭐ galunisertib (LY2157299, ALK5 inhibitor in cancer clinical development), vactosertib (TEW-7197), SB-431542 (research ALK4/5/7 inhibitor), and emerging TGF-β/activin pathway-targeted therapeutics in cancer and fibrosis.

Yes, and rescue experiments are uniquely powerful in this double knockout background: • Single-iRhom rescue: re-introduction of iRhom1 alone or iRhom2 alone in the double knockout enables paralog-specific TACE substrate selection studies — the gold-standard experimental design. • Combined rescue: simultaneous iRhom1 + iRhom2 re-expression restores ADAM17 maturation capacity and serves as the positive control. • Construct design: codon-modified RHBDF1 or RHBDF2 sequences with small C-terminal tags (FLAG, HA). Both must preserve the rhomboid family pseudoenzyme architecture. • Functional readout: rescue should restore ADAM17 Golgi maturation and substrate shedding; paralog-specific rescue reveals iRhom1-versus iRhom2-preferred substrates. HEK293's very high transfection efficiency enables systematic paralog-specific rescue experiments.