HRC Double Nickase Plasmid (m): sc-420947-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HRC 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
- HRC Double Nickase Plasmid (m) and HRC Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Hrc. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HRC Double Nickase Plasmid (m) | sc-420947-NIC | 20 µg | $410.00 | |||
HRC Double Nickase Plasmid (m2) | sc-420947-NIC-2 | 20 µg | $410.00 |
Mouse Hrc encodes the histidine-rich calcium-binding protein (HRC), a luminal sarcoplasmic reticulum component that modulates calcium storage and release dynamics in striated muscle. HRC interacts with key excitation–contraction coupling machinery, including SERCA-driven Ca2+ reuptake and ryanodine receptor-dependent Ca2+ release, thereby shaping cytosolic Ca2+ transients and downstream signaling. Through its role in calcium homeostasis, HRC is linked to pathways governing myocyte contractility, stress responses, and Ca2+-dependent transcriptional programs. Dysregulated HRC function has been associated with altered cardiac and skeletal muscle physiology and is commonly studied in the context of arrhythmogenesis and cardiomyopathy-relevant cellular phenotypes.
HRC Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Hrc locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Hrc. 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 Hrc 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 Hrc-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.