Date published: 2026-7-9

1-800-457-3801

SCBT Portrait Logo
Seach Input

Factor XIII B Double Nickase Plasmid (h): sc-403574-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
  • Factor XIII B 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
  • Factor XIII B Double Nickase Plasmid (h) and Factor XIII B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting F13B. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Factor XIII B Antibody (GMA-033): sc-65957
    Gene Editing Promo Banner

    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    Factor XIII B Double Nickase Plasmid (h)

    sc-403574-NIC
    20 µg
    $410.00

    Factor XIII B Double Nickase Plasmid (h2)

    sc-403574-NIC-2
    20 µg
    $410.00

    F13B encodes the B subunit of coagulation factor XIII, a non-catalytic carrier protein that stabilizes the A subunit (F13A1) in plasma and regulates its availability for activation during the terminal phase of the coagulation cascade. Upon thrombin and calcium-dependent activation of factor XIII, the A subunit transglutaminase cross-links fibrin and other extracellular matrix proteins, increasing clot tensile strength and resistance to fibrinolysis. Through these processes, Factor XIII B supports hemostasis and links coagulation to wound repair and matrix remodeling pathways. Genetic or functional perturbations in F13B are associated with factor XIII deficiency phenotypes and altered clot stability, making it relevant to studies of bleeding disorders and thromboinflammatory biology.

    Factor XIII B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the F13B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within F13B. 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 F13B 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 F13B-disrupted clones.

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