Date published: 2026-7-22

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CREST Double Nickase Plasmid (h): sc-403134-NIC

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CREST 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
  • CREST Double Nickase Plasmid (h) and CREST Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SS18L1. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CREST Antibody (D-7): sc-515827
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    CREST Double Nickase Plasmid (h)

    sc-403134-NIC
    20 µg
    $410.00

    CREST Double Nickase Plasmid (h2)

    sc-403134-NIC-2
    20 µg
    $410.00

    SS18L1 encodes CREST, a neuron-enriched transcriptional regulator that couples chromatin remodeling to activity-dependent gene expression. CREST interacts with the BAF (SWI/SNF) complex and corepressors such as BRG1 and HDACs to modulate neuronal differentiation programs, dendritic morphogenesis, and synaptic plasticity. Through these epigenetic and transcriptional mechanisms, CREST influences RNA processing and stress-responsive pathways that shape neuronal homeostasis. Dysregulation of CREST-linked networks has been associated with neurodegenerative phenotypes and altered neuronal connectivity, making SS18L1 a useful locus for mechanistic studies in nervous system models.

    CREST Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SS18L1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SS18L1. 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 SS18L1 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 SS18L1-disrupted clones.

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