LSm11 Double Nickase Plasmid (m): sc-428300-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LSm11 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
- LSm11 Double Nickase Plasmid (m) and LSm11 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Lsm11. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LSm11 Double Nickase Plasmid (m) | sc-428300-NIC | 20 µg | $410.00 | |||
LSm11 Double Nickase Plasmid (m2) | sc-428300-NIC-2 | 20 µg | $410.00 |
Mouse Lsm11 encodes LSm11, a core component of the U7 small nuclear ribonucleoprotein (snRNP) that is specialized for 3′ end processing of replication-dependent histone pre-mRNAs. Through its participation in the U7-dependent histone RNA processing pathway, LSm11 helps ensure proper histone transcript maturation, coupling S-phase progression to chromatin assembly and genome stability. Disruption of LSm11 function is expected to perturb histone mRNA homeostasis, with downstream effects on DNA replication stress responses and cell-cycle regulation. These processes are broadly relevant to proliferative phenotypes and to mechanistic studies of chromatin maintenance and genomic integrity in mouse cellular models.
LSm11 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Lsm11 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Lsm11. 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 Lsm11 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 Lsm11-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.