HELZ Double Nickase Plasmid (h): sc-411392-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HELZ 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
- HELZ Double Nickase Plasmid (h) and HELZ Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting HELZ. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HELZ Antibody (FA-52): sc-130438
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HELZ Double Nickase Plasmid (h) | sc-411392-NIC | 20 µg | $410.00 | |||
HELZ Double Nickase Plasmid (h2) | sc-411392-NIC-2 | 20 µg | $410.00 |
Human HELZ encodes a helicase-like RNA-binding protein with zinc finger motifs that associates with translating ribosomes and contributes to post-transcriptional gene regulation. HELZ has been linked to control of mRNA metabolism, including translation efficiency and turnover, and to broader programs governing cell growth and stress responses. Through effects on RNA processing and protein synthesis, HELZ can influence pathways that shape proliferation and differentiation states. Altered RNA regulatory networks involving HELZ have been noted in contexts relevant to tumor biology and other diseases where translational control is perturbed.
HELZ Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the HELZ locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within HELZ. 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 HELZ 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 HELZ-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.