CGRP2 Double Nickase Plasmid (h): sc-401165-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CGRP2 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
- CGRP2 Double Nickase Plasmid (h) and CGRP2 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CALCB. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CGRP2 Double Nickase Plasmid (h) | sc-401165-NIC | 20 µg | $410.00 | |||
CGRP2 Double Nickase Plasmid (h2) | sc-401165-NIC-2 | 20 µg | $410.00 |
CALCB encodes calcitonin gene-related peptide 2 (CGRP2), a neuropeptide generated by proteolytic processing that signals primarily through the calcitonin receptor-like receptor (CALCRL) in complex with receptor activity-modifying proteins (RAMPs). CGRP2 activates Gs-coupled signaling to elevate cAMP and engage downstream PKA/CREB-dependent transcriptional programs, influencing vasomotor tone, neurogenic inflammation, nociceptive transmission, and neuro-immune communication. In peripheral and central sensory pathways, CGRP-family peptides coordinate vascular and immune responses to neuronal activity and modulate synaptic excitability. Dysregulated CGRP signaling has been implicated in migraine biology, inflammatory pain states, and vascular homeostasis, making CALCB a relevant target for mechanistic studies in neurovascular and neuroinflammatory models.
CGRP2 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CALCB locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CALCB. 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 CALCB 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 CALCB-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.