ACHE Knockout HAP1 Cell Line
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Cat.No.:
EDC08152
Species:
Human
Cell Name:
HAP1
Gene:
ACHE
Gene ID:
43
Size:
1×10⁶cells
ACHE Knockout HAP1 Cell Line is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performotion Cas9 Protein and Hassle-Free Cell Selection.
| Cat.No. | EDC08152 |
|---|---|
| Product Name | ACHE Knockout HAP1 Cell Line |
| Species | Human |
| Cell Line | HAP1 |
| Cellosaurus ID | CVCL_0F62 |
| Cell Line Synonyms | Highly Aggressively Proliferating Immortalized |
| Gene ID | |
| Gene | ACHE |
| Summary |
Acetylcholinesterase hydrolyzes the neurotransmitter, acetylcholine at neuromuscular junctions and brain cholinergic synapses, and thus terminates signal transmission. It is also found on the red blood cell membranes, where it constitutes the Yt blood group antigen. Acetylcholinesterase exists in multiple molecular forms which possess similar catalytic properties, but differ in their oligomeric assembly and mode of cell attachment to the cell surface. It is encoded by the single ACHE gene, and the structural diversity in the gene products arises from alternative mRNA splicing, and post-translational associations of catalytic and structural subunits. The major form of acetylcholinesterase found in brain, muscle and other tissues is the hydrophilic species, which forms disulfide-linked oligomers with collagenous, or lipid-containing structural subunits. The other, alternatively spliced form, expressed primarily in the erythroid tissues, differs at the C-terminal end, and contains a cleavable hydrophobic peptide with a GPI-anchor site. It associates with the membranes through the phosphoinositide (PI) moieties added post-translationally. AChE activity may constitute a sensitive biomarker of RBC ageing in vivo, and thus, may be of aid in understanding the effects of transfusion[provided by RefSeq, Sep 2019]
|
| Digestion Time | 2 min |
| Morphology | Adherent |
| Passage Ratio | 1:8~1:10 |
| Complete Culture Medium | IMDM+10%FBS |
| Freezing Medium | 90%FBS+10%DMSO |
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
FAQ
Which is better for studying ACHE function, ACHE Knockout HAP1 Cell Line or ACHE overexpression HAP1 Cell Line?
The choice depends on whether you are studying ACHE (acetylcholinesterase)'s role as the principal acetylcholine-hydrolyzing enzyme or modeling its applications in Alzheimer's disease, neuromuscular biology, and nerve agent toxicology. The Knockout line is the standard tool for asking whether ACHE is required for these processes — ACHE is the enzyme that rapidly hydrolyzes the neurotransmitter acetylcholine at cholinergic synapses and neuromuscular junctions, terminating cholinergic signaling; ACHE is the target of clinically important cholinesterase inhibitors and the principal target of organophosphate nerve agents and pesticides. Overexpression is useful for studying ACHE gain-of-function effects.
For cholinergic biology research, the EDITGENE ACHE Knockout in HAP1 enables study of ACHE biology. BCHE (butyrylcholinesterase) expression analysis aids interpretation given partial functional overlap. Rescue with wild-type or catalytically-dead ACHE enables structure-function studies. The knockout is a critical specificity tool for ⭐⭐ Alzheimer's disease cholinesterase inhibitors (⭐ donepezil/Aricept, rivastigmine/Exelon, galantamine/Razadyne), myasthenia gravis treatments (pyridostigmine, neostigmine), and organophosphate/nerve agent toxicology research.
What are the application scenarios for this model?
Primary applications:
• Acetylcholine hydrolysis: ACHE enzymatic activity (Ellman assay) in ACHE-null cells.
• Cholinesterase inhibitor specificity: critical genetic control for ⭐⭐ donepezil (Aricept), rivastigmine (Exelon), galantamine (Razadyne) Alzheimer's drugs — should have no ACHE inhibition target in ACHE-null cells.
• Nerve agent/organophosphate toxicology: organophosphate (e.g., paraoxon) and nerve agent ACHE inhibition studies.
• BCHE dissection: BCHE expression analysis to interpret ACHE-specific functions given partial overlap.
EDITGENE recommends this model as a critical specificity control for Alzheimer's cholinesterase inhibitors and organophosphate toxicology research.
Is this ACHE Knockout HAP1 Cell Line compatible with overexpression rescue experiments?
Yes. ACHE rescue experiments are well-established for cholinesterase research:
• Construct design: use a codon-modified ACHE sequence with a small tag — ACHE has multiple splice variants (synaptic AChE-S/T, erythrocytic AChE-E) with different C-termini; tag placement requires care to preserve the relevant isoform.
• Catalytically-dead rescue: S203A in the catalytic serine triad abolishes acetylcholinesterase activity.
• Surface/secretion validation: confirm appropriate localization (GPI-anchored or secreted depending on isoform).
• Functional readout: rescue should restore acetylcholine hydrolysis measured by Ellman assay.
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.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.
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