LAPTM4B Double Nickase Plasmid (h): sc-408254-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LAPTM4B 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
- LAPTM4B Double Nickase Plasmid (h) and LAPTM4B Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LAPTM4B. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LAPTM4B Double Nickase Plasmid (h) | sc-408254-NIC | 20 µg | $410.00 |
LAPTM4B (lysosomal protein transmembrane 4 beta) is a multi-pass lysosomal/endosomal membrane protein that regulates intracellular trafficking, lysosome-associated signaling, and membrane dynamics. It participates in endolysosomal transport processes that influence receptor turnover and downstream pathways such as PI3K/AKT and autophagy-lysosome homeostasis, impacting cellular stress responses and nutrient sensing. Altered LAPTM4B expression has been associated with changes in proliferation, invasion, and drug handling in multiple tumor contexts, making it a relevant target for dissecting lysosome-centered mechanisms in disease models. In human cells, LAPTM4B is also studied for its roles in vesicular organization and modulation of signaling outputs from internalized receptors.
LAPTM4B Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LAPTM4B locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LAPTM4B. 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 LAPTM4B 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 LAPTM4B-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.