UTX Double Nickase Plasmid (m): sc-423635-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- UTX 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
- UTX Double Nickase Plasmid (m) and UTX Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Kdm6a. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: UTX Antibody (E-8): sc-514859
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
UTX Double Nickase Plasmid (m) | sc-423635-NIC | 20 µg | $410.00 | |||
UTX Double Nickase Plasmid (m2) | sc-423635-NIC-2 | 20 µg | $410.00 |
Mouse Kdm6a encodes UTX, a JmjC-domain histone demethylase that removes repressive H3K27me3 marks to promote transcriptional activation. UTX functions in chromatin remodeling and developmental gene regulation, coordinating lineage specification programs and broad epigenetic control of cell identity. It interfaces with enhancer and promoter regulation through interactions with COMPASS-like complexes and other transcriptional regulators, linking histone modification dynamics to differentiation and proliferation. Dysregulation of Kdm6a/UTX-dependent chromatin states has been associated with altered developmental trajectories and oncogenic transcriptional programs, making it a useful model for epigenetics and disease-relevant pathway studies.
UTX Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Kdm6a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Kdm6a. 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 Kdm6a 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 Kdm6a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.