Sprr1b Double Nickase Plasmid (m): sc-423137-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Sprr1b 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
- Sprr1b Double Nickase Plasmid (m) and Sprr1b Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Sprr1b. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Sprr1b Double Nickase Plasmid (m) | sc-423137-NIC | 20 µg | $410.00 | |||
Sprr1b Double Nickase Plasmid (m2) | sc-423137-NIC-2 | 20 µg | $410.00 |
Sprr1b (small proline-rich protein 1B) is a mouse cornified envelope precursor that becomes crosslinked by transglutaminases during terminal keratinocyte differentiation, contributing to epidermal barrier formation and mechanical resilience. Its expression is induced downstream of epithelial stress and differentiation cues, and it is frequently used as a marker of squamous differentiation programs that involve EGFR/MAPK and AP-1–regulated transcriptional responses. Beyond skin, Sprr1b can be upregulated in injured epithelia and regenerating tissues, reflecting roles in barrier repair and cellular adaptation to damage. Dysregulated SPRR-family expression has been associated with hyperkeratotic and inflammatory skin states as well as epithelial remodeling contexts, making Sprr1b relevant for studies of barrier dysfunction and epithelial stress biology.
Sprr1b Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Sprr1b locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Sprr1b. 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 Sprr1b 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 Sprr1b-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.