Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
ICAM-1/CD54 Double Nickase Plasmid (h): sc-400098-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ICAM-1/CD54 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
- ICAM-1/CD54 Double Nickase Plasmid (h) and ICAM-1/CD54 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting ICAM1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ICAM-1/CD54 Antibody (G-5): sc-8439
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ICAM-1/CD54 Double Nickase Plasmid (h) | sc-400098-NIC | 20 µg | $410.00 | |||
ICAM-1/CD54 Double Nickase Plasmid (h2) | sc-400098-NIC-2 | 20 µg | $410.00 |
ICAM1 encodes intercellular adhesion molecule 1 (ICAM-1/CD54), an inducible immunoglobulin superfamily receptor expressed on endothelial cells and multiple leukocyte subsets that supports firm adhesion and transmigration of immune cells. ICAM-1 binds integrins such as LFA-1 (ITGAL/ITGB2) and MAC-1 (ITGAM/ITGB2), coupling cytokine-driven activation programs to leukocyte arrest, diapedesis, and immunological synapse stability. Its expression is strongly regulated by inflammatory signaling, including NF-κB and MAPK pathways downstream of TNF-α, IL-1, and pattern-recognition receptors, and contributes to endothelial activation and tissue immune infiltration. Dysregulated ICAM1 is associated with chronic inflammatory states, vascular inflammation, and tumor–immune interactions, making it a widely used marker and mechanistic node for studying leukocyte trafficking and inflammatory microenvironments.
ICAM-1/CD54 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the ICAM1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within ICAM1. 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 ICAM1 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 ICAM1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.