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.
Sulf-2 Double Nickase Plasmid (m2): sc-428206-NIC-2
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Sulf-2 Double Nickase Plasmid (m2) 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
- Sulf-2 Double Nickase Plasmid (m2) and Sulf-2 Double Nickase Plasmid (m22) encode distinct paired gRNA designs targeting Sulf2. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Sulf-2 Antibody (G-4): sc-271772
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Sulf-2 Double Nickase Plasmid (m2) | sc-428206-NIC-2 | 20 µg | $410.00 |
Mouse Sulf2 encodes extracellular heparan sulfate 6-O-endosulfatase 2 (Sulf-2), a secreted enzyme that remodels cell-surface and matrix heparan sulfate by removing 6-O-sulfate groups and thereby modulating ligand availability and receptor interactions. By editing heparan sulfate sulfation patterns, Sulf-2 influences key signaling axes including FGF, WNT, Hedgehog, BMP, and chemokine gradients, shaping processes such as cell migration, tissue patterning, angiogenesis, and inflammatory responses. Dysregulated SULF2 activity has been linked to altered extracellular matrix dynamics and aberrant signaling in contexts such as tumor biology, fibrosis, and neurodevelopmental phenotypes, making Sulf2 a useful target for mechanistic studies of glycosaminoglycan-dependent signaling. Gene editing of Sulf2 in mouse models enables functional dissection of sulfation-dependent pathway tuning, extracellular niche regulation, and disease-relevant microenvironmental interactions in vitro and in vivo.
Sulf-2 Double Nickase Plasmid (m2) consists of a matched pair of plasmids engineered for high-specificity editing of the Sulf2 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Sulf2. 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 Sulf2 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 Sulf2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.