RHAMM Double Nickase Plasmid (h): sc-402431-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RHAMM 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
- RHAMM Double Nickase Plasmid (h) and RHAMM Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HMMR. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RHAMM Antibody (H-8): sc-515221
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RHAMM Double Nickase Plasmid (h) | sc-402431-NIC | 20 µg | $410.00 | |||
RHAMM Double Nickase Plasmid (h2) | sc-402431-NIC-2 | 20 µg | $410.00 |
Human HMMR encodes RHAMM (receptor for hyaluronan-mediated motility), a hyaluronan-binding protein that localizes to the cell surface, cytoplasm, and mitotic spindle to coordinate cell motility and proliferation. RHAMM integrates extracellular matrix–hyaluronan cues with cytoskeletal remodeling, centrosome/spindle organization, and MAPK/ERK-associated signaling that supports cell-cycle progression and migration. Dysregulated HMMR/RHAMM expression and localization have been linked to altered mitotic fidelity, invasive behavior, and tumor-associated phenotypes in multiple cancer contexts. As a result, HMMR is widely studied in pathways governing extracellular matrix signaling, epithelial–mesenchymal-like transitions, and mitosis-related genomic stability.
RHAMM Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HMMR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HMMR. 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 HMMR 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 HMMR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.