CDK5RAP3 Double Nickase Plasmid (h): sc-408965-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CDK5RAP3 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
- CDK5RAP3 Double Nickase Plasmid (h) and CDK5RAP3 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CDK5RAP3. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CDK5RAP3 Antibody (E-7): sc-271776
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CDK5RAP3 Double Nickase Plasmid (h) | sc-408965-NIC | 20 µg | $410.00 | |||
CDK5RAP3 Double Nickase Plasmid (h2) | sc-408965-NIC-2 | 20 µg | $410.00 |
CDK5RAP3 (also known as C53/LZAP) is a multifunctional adaptor protein implicated in the regulation of cell-cycle progression, stress responses, and intracellular signaling. It has been linked to modulation of NF-κB signaling and interactions with ubiquitin-dependent protein quality control pathways, influencing transcriptional outputs and proteostasis. CDK5RAP3 also participates in endoplasmic reticulum homeostasis and autophagy-related processes, connecting cellular stress sensing to growth control. Dysregulated CDK5RAP3 expression or function has been associated with altered proliferation and survival phenotypes reported in cancer biology and inflammation-related research contexts.
CDK5RAP3 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CDK5RAP3 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CDK5RAP3. 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 CDK5RAP3 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 CDK5RAP3-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.