Date published: 2026-7-16

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TC-PTP Double Nickase Plasmid (m): sc-422509-NIC

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • TC-PTP 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
  • TC-PTP Double Nickase Plasmid (m) and TC-PTP Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ptpn2. One or both designs may be available
  • Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: TC-PTP Antibody (D-3): sc-398997
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    TC-PTP Double Nickase Plasmid (m)

    sc-422509-NIC
    20 µg
    $410.00

    Mouse Ptpn2 encodes T cell protein tyrosine phosphatase (TC-PTP), a non-receptor phosphatase that attenuates signaling from cytokine and growth factor receptors by dephosphorylating key substrates such as JAKs and STATs. Through regulation of JAK/STAT and related immune signaling networks, TC-PTP helps set thresholds for inflammatory responses, T cell activation, and epithelial homeostasis. Ptpn2 activity also intersects with insulin receptor signaling and stress-response pathways that influence cellular metabolism and proliferation. Genetic and functional studies implicate altered PTPN2/TC-PTP signaling in autoimmune and inflammatory phenotypes, cancer-relevant immune evasion contexts, and metabolic dysregulation, making it a valuable target for mechanistic investigations.

    TC-PTP Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ptpn2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ptpn2. 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 Ptpn2 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 Ptpn2-disrupted clones.

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