ABCG1 Double Nickase Plasmid (m): sc-418933-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ABCG1 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
- ABCG1 Double Nickase Plasmid (m) and ABCG1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Abcg1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ABCG1 Double Nickase Plasmid (m) | sc-418933-NIC | 20 µg | $410.00 | |||
ABCG1 Double Nickase Plasmid (m2) | sc-418933-NIC-2 | 20 µg | $410.00 |
Mouse Abcg1 encodes the ATP-binding cassette transporter ABCG1, a key regulator of intracellular lipid homeostasis that promotes cholesterol and phospholipid efflux to extracellular acceptors such as HDL. ABCG1 operates within macrophages, endothelial cells, and other metabolically active tissues to coordinate membrane lipid composition, lipid droplet dynamics, and inflammatory signaling. Through crosstalk with LXR-dependent transcriptional programs and pathways governing foam cell formation, ABCG1 influences reverse cholesterol transport and innate immune responses. Dysregulated Abcg1 activity has been linked to altered atherogenic lipid handling, pulmonary lipid accumulation, and metabolic inflammation in preclinical models.
ABCG1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Abcg1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Abcg1. 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 Abcg1 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 Abcg1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.