MCC Double Nickase Plasmid (h): sc-404248-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MCC 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
- MCC Double Nickase Plasmid (h) and MCC Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MCC. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MCC Antibody (A-9): sc-398216
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MCC Double Nickase Plasmid (h) | sc-404248-NIC | 20 µg | $410.00 | |||
MCC Double Nickase Plasmid (h2) | sc-404248-NIC-2 | 20 µg | $410.00 |
Human MCC encodes the Mutated in Colorectal Cancers protein, a cytoplasmic and nuclear factor implicated in regulation of cell-cycle progression, differentiation, and epithelial tissue homeostasis. MCC has been linked to Wnt/β-catenin–associated processes and transcriptional control, with reported roles in constraining proliferative signaling and coordinating checkpoint-related responses. Altered MCC expression or mutation is observed in multiple tumor types, including colorectal cancer, and has been associated with changes in migration, polarity, and genomic stability phenotypes relevant to oncogenic transformation. As a research target, MCC enables mechanistic interrogation of signaling networks that couple transcriptional programs to proliferation and tissue architecture.
MCC Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MCC locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MCC. 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 MCC 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 MCC-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.