Sab Double Nickase Plasmid (h): sc-405461-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Sab 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
- Sab Double Nickase Plasmid (h) and Sab Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting SH3BP5. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Sab Antibody (A-3): sc-390512
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Sab Double Nickase Plasmid (h) | sc-405461-NIC | 20 µg | $410.00 |
SH3BP5 encodes Sab, a mitochondrial outer membrane scaffold that binds stress-activated kinases and helps organize JNK signaling at the mitochondria. Through regulating kinase localization and crosstalk with MAPK-dependent stress responses, Sab influences mitochondrial function, redox balance, and apoptosis-related signaling. Altered Sab/JNK pathway activity has been linked to cellular injury responses and is studied in contexts of metabolic stress, inflammatory signaling, and neurodegeneration-relevant mitochondrial dysfunction. As a node connecting cytosolic stress cues to mitochondrial outcomes, SH3BP5 is routinely investigated for its impact on mitochondrial dynamics and cell fate decisions.
Sab Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the SH3BP5 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within SH3BP5. 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 SH3BP5 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 SH3BP5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.