Date published: 2026-9-8

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ALP CRISPR/Cas9 KO Plasmid (h): sc-401877

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ALP 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 ALP 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: ALP Antibody (B-10): sc-365765
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ALP CRISPR/Cas9 KO Plasmid (h)

    sc-401877
    20 µg
    $397.00

    Overview

    PDLIM3 encodes ALP (actinin-associated LIM protein), a PDZ-LIM family adaptor enriched in striated muscle that localizes to the Z-disc and links α-actinin–based actin filaments to signaling complexes. Through its PDZ and LIM domains, ALP supports sarcomere assembly, mechanotransduction, and cytoskeletal organization by scaffolding protein interactions that coordinate actin dynamics and stress-responsive pathways. Altered PDLIM3 expression or disruption of Z-disc integrity is associated with impaired myofibrillar architecture and has been studied in the context of cardiomyopathy and skeletal muscle dysfunction. As a marker of muscle structural homeostasis, ALP is relevant for investigating how cytoskeletal scaffolds tune contractile function, cell adhesion, and stress signaling.

    ALP CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PDLIM3 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PDLIM3 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 PDLIM3 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 ALP protein expression.

    This CRISPR knockout system enables efficient generation of PDLIM3-deficient cell models for investigation of ALP signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting PDLIM3 exon(s) critical for ALP 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 PDLIM3 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by ALP CRISPR/Cas9 KO Plasmid (h) and ALP CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PDLIM3 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by ALP HDR Plasmid (h) and ALP HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PDLIM3 homology arms to support homology-directed repair at defined PDLIM3 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.