Limd1 Double Nickase Plasmid (h): sc-404413-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Limd1 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
- Limd1 Double Nickase Plasmid (h) and Limd1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting LIMD1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Limd1 Antibody (H-4): sc-271448
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Limd1 Double Nickase Plasmid (h) | sc-404413-NIC | 20 µg | $410.00 | |||
Limd1 Double Nickase Plasmid (h2) | sc-404413-NIC-2 | 20 µg | $410.00 |
LIMD1 encodes Limd1, a LIM domain–containing adaptor protein that functions as a scaffold in the nucleus and cytoplasm to coordinate protein–protein interactions. Limd1 has been linked to transcriptional control and signal integration at growth-regulatory nodes, including Hippo pathway regulation through interactions that influence YAP/TAZ activity. Through these roles, LIMD1 contributes to control of cell proliferation, adhesion, and stress-responsive gene expression programs. Altered LIMD1 expression or genomic loss has been associated with tumorigenesis-related phenotypes in multiple tissue contexts, making it a useful target for mechanistic studies of growth control and pathway crosstalk.
Limd1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the LIMD1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within LIMD1. 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 LIMD1 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 LIMD1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.