LSm11 Double Nickase Plasmid (h): sc-406646-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LSm11 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
- LSm11 Double Nickase Plasmid (h) and LSm11 Double Nickase Plasmid (h2) 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 (h) | sc-406646-NIC | 20 µg | $410.00 | |||
LSm11 Double Nickase Plasmid (h2) | sc-406646-NIC-2 | 20 µg | $410.00 |
LSM11 encodes LSm11, an Sm-like RNA-binding protein that forms part of the U7 small nuclear ribonucleoprotein (U7 snRNP) specialized for 3′ end processing of replication-dependent histone pre-mRNAs. Through interactions with U7 snRNA and associated factors such as the FLASH/NPAT axis, LSm11 supports S-phase–linked histone gene expression, chromatin assembly, and genome stability during cell-cycle progression. Disruption of this pathway can perturb histone supply, replication timing, and DNA damage responses, processes frequently examined in proliferative stress and oncogenic contexts. LSm11 is therefore relevant for mechanistic studies of RNA processing–coupled cell-cycle regulation and the consequences of histone mRNA misprocessing.
LSm11 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LSM11 locus in human 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.