HSPA2 Double Nickase Plasmid (h): sc-400832-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HSPA2 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
- HSPA2 Double Nickase Plasmid (h) and HSPA2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HSPA2. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HSPA2 Double Nickase Plasmid (h) | sc-400832-NIC | 20 µg | $410.00 | |||
HSPA2 Double Nickase Plasmid (h2) | sc-400832-NIC-2 | 20 µg | $410.00 |
HSPA2 encodes a cytosolic HSP70 family molecular chaperone that promotes ATP-dependent protein folding, refolding of stress-denatured substrates, and quality control through interactions with co-chaperones and ubiquitin–proteasome components. In human cells, HSPA2 supports proteostasis under basal and stress conditions, influencing pathways linked to heat shock response, cell-cycle progression, and maintenance of protein complex assembly. Expression and functional perturbation of HSPA2 have been studied in contexts including germ cell biology and tumor cell proteostasis, where altered chaperone activity can affect survival signaling and stress adaptation. As a nodal regulator of proteome integrity, HSPA2 is a useful target for mechanistic studies of folding stress, aggregation control, and chaperone network rewiring.
HSPA2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HSPA2 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HSPA2. 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 HSPA2 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 HSPA2-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.