Date published: 2026-7-7

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AChE CRISPR/Cas9 KO Plasmid (h): sc-401091

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • AChE CRISPR/Cas9 Knockout (KO) Plasmid (h) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
  • gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the AChE genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
  • The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: AChE Antibody (A-11): sc-373901
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    AChE CRISPR/Cas9 KO Plasmid (h)

    sc-401091
    20 µg
    $397.00

    Overview

    Human ACHE encodes acetylcholinesterase (AChE), a serine hydrolase that terminates cholinergic neurotransmission by rapidly hydrolyzing acetylcholine at synapses and neuromuscular junctions. Beyond canonical synaptic signaling, AChE activity influences excitation–contraction coupling, autonomic regulation, and cholinergic anti-inflammatory signaling through modulation of acetylcholine availability. ACHE expression and enzymatic dysregulation have been linked to altered neuronal network function, stress and neuroinflammation-associated pathways, and susceptibility to neuromuscular and neurodegenerative phenotypes. As a membrane-tethered and soluble enzyme with tissue-specific isoforms, ACHE is frequently studied in models of synaptic physiology, toxicant response, and cholinergic signaling crosstalk.

    AChE CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ACHE gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ACHE together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.

    The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the ACHE open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish AChE protein expression.

    This CRISPR knockout system enables efficient generation of ACHE-deficient cell models for investigation of AChE signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting ACHE exon(s) critical for AChE function
    • Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
    • GFP reporter for identification of transfected cells
    • Pool of plasmids targeting multiple ACHE genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by AChE CRISPR/Cas9 KO Plasmid (h) and AChE CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ACHE locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by AChE HDR Plasmid (h) and AChE HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ACHE homology arms to support homology-directed repair at defined ACHE target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.

    For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.