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.
LSD1 Double Nickase Plasmid (m): sc-430289-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- LSD1 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
- LSD1 Double Nickase Plasmid (m) and LSD1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Kdm1a. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: LSD1 Antibody (B-9): sc-271720
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LSD1 Double Nickase Plasmid (m) | sc-430289-NIC | 20 µg | $410.00 | |||
LSD1 Double Nickase Plasmid (m2) | sc-430289-NIC-2 | 20 µg | $410.00 |
Mouse Kdm1a encodes lysine-specific demethylase 1 (LSD1), a FAD-dependent chromatin enzyme that removes mono- and dimethyl marks from H3K4 and, in certain contexts, H3K9. Through interactions with CoREST/HDAC and other transcriptional coregulator complexes, LSD1 coordinates enhancer and promoter states that control lineage commitment, cell-cycle programs, and differentiation. LSD1 activity links epigenetic remodeling to signaling and transcriptional networks that govern stem cell maintenance, neurodevelopmental gene expression, and immune cell maturation. Dysregulation of LSD1-dependent chromatin repression or activation has been associated with aberrant proliferation and altered differentiation states across multiple disease-relevant biological models, supporting its use as a mechanistic node in epigenetics research.
LSD1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Kdm1a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Kdm1a. 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 Kdm1a 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 Kdm1a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.