Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
UCMA Double Nickase Plasmid (h): sc-406716-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- UCMA 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
- UCMA Double Nickase Plasmid (h) and UCMA Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting UCMA. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: UCMA Antibody (H-2): sc-515468
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
UCMA Double Nickase Plasmid (h) | sc-406716-NIC | 20 µg | $410.00 | |||
UCMA Double Nickase Plasmid (h2) | sc-406716-NIC-2 | 20 µg | $410.00 |
UCMA (upper zone of growth plate and cartilage matrix associated) encodes a vitamin K–dependent, secreted extracellular matrix protein also known as Gla-rich protein (GRP) that is enriched in cartilage and vascular tissues. UCMA undergoes γ-carboxylation of glutamate residues, a post-translational modification that supports calcium binding and links UCMA to extracellular mineral homeostasis and matrix organization. In musculoskeletal biology, UCMA is associated with chondrocyte differentiation, growth plate maturation, and cartilage matrix integrity, intersecting with signaling programs that coordinate endochondral ossification and tissue remodeling. Dysregulated UCMA expression and/or altered carboxylation status has been reported in contexts of abnormal calcification, cartilage degeneration, and inflammatory joint disease, making it relevant for mechanistic studies of matrix-driven pathology.
UCMA Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the UCMA locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within UCMA. 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 UCMA 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 UCMA-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.