MUTYH Double Nickase Plasmid (h): sc-404076-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MUTYH 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
- MUTYH Double Nickase Plasmid (h) and MUTYH Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MUTYH. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MUTYH Antibody (C-6): sc-374571
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MUTYH Double Nickase Plasmid (h) | sc-404076-NIC | 20 µg | $410.00 | |||
MUTYH Double Nickase Plasmid (h2) | sc-404076-NIC-2 | 20 µg | $410.00 |
MUTYH encodes a DNA glycosylase that initiates base excision repair by recognizing and excising adenines mispaired with 8-oxo-7,8-dihydroguanine, thereby limiting G:C→T:A transversions caused by oxidative DNA damage. This activity contributes to genome maintenance during replication and interfaces with downstream BER factors and replication-associated repair processes to preserve chromosomal integrity. Disruption or reduced function of MUTYH is linked to elevated mutational burden and genomic instability, with strong relevance to colorectal tumor predisposition and related DNA repair–defect phenotypes. As a result, MUTYH is frequently studied in oxidative stress responses, mutation avoidance pathways, and mechanisms shaping somatic mutation signatures.
MUTYH Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MUTYH locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MUTYH. 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 MUTYH 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 MUTYH-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.