C11orf51 Double Nickase Plasmid (h): sc-407279-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C11orf51 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
- C11orf51 Double Nickase Plasmid (h) and C11orf51 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ANAPC15. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C11orf51 Double Nickase Plasmid (h) | sc-407279-NIC | 20 µg | $410.00 | |||
C11orf51 Double Nickase Plasmid (h2) | sc-407279-NIC-2 | 20 µg | $410.00 |
ANAPC15 (also annotated as C11orf51) encodes a small regulatory subunit of the anaphase-promoting complex/cyclosome (APC/C), an E3 ubiquitin ligase that coordinates orderly progression through mitosis and G1 by targeting key cell-cycle regulators for proteasomal degradation. Through APC/C-dependent ubiquitination, ANAPC15 contributes to checkpoint control, timely anaphase onset, and maintenance of genome stability. Dysregulation of APC/C composition or activity is broadly linked to chromosomal instability phenotypes relevant to proliferative disorders and cancer biology, making ANAPC15 a useful target for dissecting mitotic control mechanisms. In human cells, perturbing ANAPC15 provides a tractable entry point to study ubiquitin–proteasome signaling, spindle checkpoint dynamics, and cell-cycle timing.
C11orf51 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ANAPC15 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ANAPC15. 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 ANAPC15 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 ANAPC15-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.