ASPP1 Double Nickase Plasmid (m): sc-423473-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ASPP1 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
- ASPP1 Double Nickase Plasmid (m) and ASPP1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Ppp1r13b. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ASPP1 Antibody (LX011): sc-53903
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ASPP1 Double Nickase Plasmid (m) | sc-423473-NIC | 20 µg | $410.00 |
Mouse Ppp1r13b encodes apoptosis-stimulating protein of p53 1 (ASPP1), a nuclear regulator that modulates transcriptional programs controlling apoptosis, cell-cycle checkpoints, and stress responses. ASPP1 interacts with p53 family members and influences expression of pro-apoptotic targets, linking it to DNA damage signaling and chromatin-associated transcriptional control. Through these interactions, ASPP1 contributes to cellular fate decisions relevant to tumor suppression, genomic stability, and tissue homeostasis. Dysregulated ASPP1 activity or expression has been associated with altered apoptotic thresholds and cancer-related phenotypes, supporting its study in oncogenic pathways and response-to-damage networks.
ASPP1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Ppp1r13b locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Ppp1r13b. 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 Ppp1r13b 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 Ppp1r13b-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.