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.
HB9 Double Nickase Plasmid (h): sc-402097-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HB9 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
- HB9 Double Nickase Plasmid (h) and HB9 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MNX1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HB9 Antibody (F-5): sc-515769
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HB9 Double Nickase Plasmid (h) | sc-402097-NIC | 20 µg | $410.00 | |||
HB9 Double Nickase Plasmid (h2) | sc-402097-NIC-2 | 20 µg | $410.00 |
MNX1 encodes the homeobox transcription factor HB9, a sequence-specific DNA-binding regulator essential for ventral spinal cord patterning and motor neuron differentiation during development. HB9 integrates with transcriptional programs downstream of morphogen signaling and cooperates with other homeodomain factors to establish neuronal subtype identity, axon guidance properties, and maturation of motor circuits. In hematopoietic contexts, dysregulated MNX1 expression and chromosomal rearrangements involving this locus have been associated with acute leukemias, highlighting its relevance to aberrant lineage specification and transcriptional control. As a developmental regulator, MNX1 is frequently studied in models of neurogenesis, cell fate determination, and disease-associated transcriptional misregulation.
HB9 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MNX1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MNX1. 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 MNX1 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 MNX1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.