Date published: 2026-8-25

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CDKAL1 Double Nickase Plasmid (m): sc-427224-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CDKAL1 Double Nickase Plasmid (m) 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
  • CDKAL1 Double Nickase Plasmid (m) and CDKAL1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Cdkal1. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CDKAL1 Antibody (E-9): sc-393447
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    CDKAL1 Double Nickase Plasmid (m)

    sc-427224-NIC
    20 µg
    $410.00

    Mouse Cdkal1 encodes CDKAL1, a methylthiotransferase that modifies tRNALys(UUU) at position 37 (ms2t6A37), supporting accurate decoding of lysine codons during translation. By maintaining translational fidelity, CDKAL1 influences proteostasis and cellular stress responses, with particular relevance to secretory cell function and metabolic regulation. Genetic and functional studies link CDKAL1 to glucose homeostasis and pancreatic β-cell performance, making it a frequently studied locus in diabetes-associated pathways. In murine systems, Cdkal1 perturbation is used to examine how tRNA modification impacts protein synthesis, ER stress, and downstream metabolic phenotypes.

    CDKAL1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Cdkal1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cdkal1. 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 Cdkal1 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 Cdkal1-disrupted clones.

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