JMJD3 Double Nickase Plasmid (m): sc-432132-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- JMJD3 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
- JMJD3 Double Nickase Plasmid (m) and JMJD3 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Kdm6b. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
JMJD3 Double Nickase Plasmid (m) | sc-432132-NIC | 20 µg | $410.00 | |||
JMJD3 Double Nickase Plasmid (m2) | sc-432132-NIC-2 | 20 µg | $410.00 |
Mouse Kdm6b encodes JMJD3 (KDM6B), a Jumonji C domain–containing histone demethylase that removes repressive H3K27me3 marks to promote transcriptional activation. JMJD3 coordinates chromatin remodeling during lineage commitment and inflammatory signaling, influencing programs downstream of pathways such as NF-κB and developmental transcriptional networks. By regulating enhancer and promoter accessibility, it contributes to macrophage polarization, neural and skeletal differentiation, and cellular senescence-related gene expression. Dysregulated Kdm6b/JMJD3 activity has been associated with altered epigenetic states observed in cancer biology, neurodevelopmental processes, and immune-mediated disease models.
JMJD3 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Kdm6b locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Kdm6b. 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 Kdm6b 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 Kdm6b-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.