Mex3a Double Nickase Plasmid (h): sc-409353-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Mex3a 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
- Mex3a Double Nickase Plasmid (h) and Mex3a Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting MEX3A. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Mex3a Double Nickase Plasmid (h) | sc-409353-NIC | 20 µg | $410.00 | |||
Mex3a Double Nickase Plasmid (h2) | sc-409353-NIC-2 | 20 µg | $410.00 |
Human MEX3A encodes Mex3a, an RNA-binding protein containing KH domains and a C3H1-type RING finger that couples post-transcriptional regulation with ubiquitin-associated control of target proteins. Mex3a influences mRNA stability, localization, and translation, thereby shaping programs linked to cell fate decisions, proliferation, and stress-adaptive responses. It has been connected to regulation of stem-like properties and epithelial homeostasis, and altered MEX3A expression has been observed in several disease-relevant contexts, including oncogenic signaling networks. As a result, MEX3A serves as a useful node for dissecting RNA regulatory circuits and proteostasis pathways in human cells.
Mex3a Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the MEX3A locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within MEX3A. 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 MEX3A 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 MEX3A-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.