CRF-RI Double Nickase Plasmid (h): sc-400730-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CRF-RI 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
- CRF-RI Double Nickase Plasmid (h) and CRF-RI Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CRHR1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CRF-RI Double Nickase Plasmid (h) | sc-400730-NIC | 20 µg | $410.00 | |||
CRF-RI Double Nickase Plasmid (h2) | sc-400730-NIC-2 | 20 µg | $410.00 |
Human CRHR1 encodes corticotropin-releasing hormone receptor 1 (CRF-RI), a class B GPCR that binds CRH peptides to initiate stress-responsive signaling. Ligand engagement primarily activates Gs/adenylyl cyclase–cAMP–PKA cascades and can couple to additional pathways such as MAPK/ERK, shaping transcriptional programs that regulate endocrine output, neuronal excitability, and immune modulation. CRF-RI signaling interfaces with the hypothalamic–pituitary–adrenal axis and broader neuroendocrine homeostasis, linking receptor activity to cellular adaptations under stress. Dysregulated CRHR1 expression or signaling has been associated with altered stress reactivity and neuropsychiatric phenotypes, supporting mechanistic studies in relevant neuronal and peripheral cell models.
CRF-RI Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CRHR1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CRHR1. 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 CRHR1 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 CRHR1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.