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.
Mast Cell Chymase Double Nickase Plasmid (h): sc-403686-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Mast Cell Chymase 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
- Mast Cell Chymase Double Nickase Plasmid (h) and Mast Cell Chymase Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CMA1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Mast Cell Chymase Antibody (CC1): sc-59586
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Mast Cell Chymase Double Nickase Plasmid (h) | sc-403686-NIC | 20 µg | $410.00 | |||
Mast Cell Chymase Double Nickase Plasmid (h2) | sc-403686-NIC-2 | 20 µg | $410.00 |
CMA1 encodes mast cell chymase, a granule-associated serine protease released during mast cell degranulation that shapes inflammatory and tissue-remodeling responses. Human chymase contributes to extracellular matrix turnover and local signaling by processing diverse substrates, including vasoactive peptides and cytokine precursors, thereby influencing protease-activated and renin–angiotensin-related pathways in the perivascular microenvironment. Dysregulated chymase activity has been linked to allergic inflammation and chronic fibrotic remodeling processes, where mast cell–derived proteases modulate leukocyte recruitment, vascular permeability, and stromal cell activation. As such, CMA1 is frequently studied in airway and cardiovascular biology, fibroinflammatory signaling networks, and mechanisms of mast cell–driven pathology.
Mast Cell Chymase Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CMA1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CMA1. 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 CMA1 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 CMA1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.