Date published: 2026-7-10

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pICln Double Nickase Plasmid (h): sc-405798-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • pICln Double Nickase Plasmid (h) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
  • Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
  • One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
  • pICln Double Nickase Plasmid (h) and pICln Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CLNS1A. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: pICln Antibody (G-1): sc-271327
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    pICln Double Nickase Plasmid (h)

    sc-405798-NIC
    20 µg
    $410.00

    pICln Double Nickase Plasmid (h2)

    sc-405798-NIC-2
    20 µg
    $410.00

    CLNS1A encodes pICln, a conserved RNA-binding protein that functions as an assembly chaperone for Sm-class ribonucleoproteins, supporting the biogenesis of spliceosomal snRNPs and other RNP complexes. Through interactions with PRMT5-containing methylosome components and Sm proteins, pICln helps coordinate arginine methylation and ordered RNP assembly, linking it to RNA splicing control and broader gene expression regulation. Altered CLNS1A/pICln function has been associated with defects in snRNP maturation, transcriptome dysregulation, and cellular stress phenotypes relevant to mechanistic studies of splicing-related disease processes.

    pICln Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CLNS1A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CLNS1A. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt CLNS1A function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.

    To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of CLNS1A-disrupted clones.

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