ASXL1 Double Nickase Plasmid (m): sc-432808-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ASXL1 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
- ASXL1 Double Nickase Plasmid (m) and ASXL1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Asxl1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: ASXL1 Antibody (6E2): sc-293204
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ASXL1 Double Nickase Plasmid (m) | sc-432808-NIC | 20 µg | $410.00 | |||
ASXL1 Double Nickase Plasmid (m2) | sc-432808-NIC-2 | 20 µg | $410.00 |
Asxl1 encodes ASXL1, a chromatin-associated regulator that cooperates with Polycomb and Trithorax group complexes to shape epigenetic states and transcriptional programs in mouse cells. ASXL1 influences histone modification dynamics, including pathways linked to H3K27 methylation and broader chromatin remodeling, thereby impacting lineage specification, proliferation, and differentiation. Perturbation of ASXL1-mediated epigenetic control alters gene expression networks involved in hematopoietic development and stem cell maintenance. Dysregulation of ASXL1 is widely studied in the context of myeloid malignancy–associated mechanisms and developmental biology, supporting its relevance for modeling disease-linked transcriptional and chromatin defects.
ASXL1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Asxl1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Asxl1. 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 Asxl1 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 Asxl1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.