Date published: 2026-9-1

1-800-457-3801

SCBT Portrait Logo
Seach Input

CDKN2B/p15 INK4B Double Nickase Plasmid (h): sc-400570-NIC

0.0(0)
Write a reviewAsk a question

Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • CDKN2B/p15 INK4B 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
  • CDKN2B/p15 INK4B Double Nickase Plasmid (h) and CDKN2B/p15 INK4B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDKN2B. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CDKN2B/p15 INK4B Antibody (D-12): sc-271791
    Gene Editing Promo Banner

    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    CDKN2B/p15 INK4B Double Nickase Plasmid (h)

    sc-400570-NIC
    20 µg
    $410.00

    CDKN2B/p15 INK4B Double Nickase Plasmid (h2)

    sc-400570-NIC-2
    20 µg
    $410.00

    CDKN2B encodes p15 INK4B, a cyclin-dependent kinase inhibitor that binds CDK4/6 to restrain RB phosphorylation and enforce the G1/S checkpoint. As a core node of cell-cycle control, CDKN2B integrates signals from antiproliferative pathways such as TGF-β/SMAD and broader senescence programs that limit inappropriate proliferation. Altered CDKN2B regulation, including deletion, promoter methylation, or locus disruption at 9p21, is frequently associated with loss of growth control in diverse malignancies and with phenotypes linked to aberrant proliferation. This biology makes CDKN2B a useful target for studying checkpoint enforcement, senescence bypass, and pathway interactions that converge on CDK4/6–RB signaling.

    CDKN2B/p15 INK4B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDKN2B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDKN2B. 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 CDKN2B 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 CDKN2B-disrupted clones.

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