KDEL receptor 1 Double Nickase Plasmid (h): sc-402751-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- KDEL receptor 1 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
- KDEL receptor 1 Double Nickase Plasmid (h) and KDEL receptor 1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting KDELR1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
KDEL receptor 1 Double Nickase Plasmid (h) | sc-402751-NIC | 20 µg | $410.00 | |||
KDEL receptor 1 Double Nickase Plasmid (h2) | sc-402751-NIC-2 | 20 µg | $410.00 |
KDELR1 encodes KDEL receptor 1, a key Golgi-to-ER retrieval receptor that recognizes KDEL-bearing soluble ER proteins and maintains ER proteostasis. By coupling ligand binding in the Golgi to COPI-mediated retrograde trafficking and pH-dependent release in the ER, KDELR1 helps regulate the early secretory pathway, ER quality control, and stress-adaptive signaling. Perturbation of KDELR1 function can disrupt protein sorting and secretory homeostasis, impacting processes such as unfolded protein response dynamics and intracellular trafficking fidelity. Altered ER–Golgi transport and proteostasis pathways are broadly relevant to research on cellular stress, immune signaling, and diverse protein-misfolding–associated phenotypes.
KDEL receptor 1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the KDELR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within KDELR1. 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 KDELR1 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 KDELR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.