JMJD2D Double Nickase Plasmid (h): sc-404743-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- JMJD2D 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
- JMJD2D Double Nickase Plasmid (h) and JMJD2D Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KDM4D. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
JMJD2D Double Nickase Plasmid (h) | sc-404743-NIC | 20 µg | $410.00 | |||
JMJD2D Double Nickase Plasmid (h2) | sc-404743-NIC-2 | 20 µg | $410.00 |
Human KDM4D (JMJD2D) encodes a Jumonji C (JmjC) domain–containing histone lysine demethylase that primarily removes repressive H3K9me2/3 marks to modulate chromatin accessibility and transcriptional programs. By reshaping local epigenetic states, JMJD2D influences DNA damage responses, cell-cycle progression, and replication-associated chromatin dynamics, interfacing with pathways that coordinate genome stability and transcription factor occupancy. Altered regulation of KDM4D has been associated with aberrant epigenetic remodeling observed in cancer-related transcriptional networks and other disorders linked to dysregulated chromatin modification. As a model epigenetic regulator, JMJD2D is frequently studied to dissect how histone demethylation impacts gene expression, chromatin structure, and stress-responsive signaling.
JMJD2D Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KDM4D locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KDM4D. 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 KDM4D 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 KDM4D-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.