GHRH-R Double Nickase Plasmid (h): sc-404197-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GHRH-R 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
- GHRH-R Double Nickase Plasmid (h) and GHRH-R Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GHRHR. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GHRH-R Double Nickase Plasmid (h) | sc-404197-NIC | 20 µg | $410.00 | |||
GHRH-R Double Nickase Plasmid (h2) | sc-404197-NIC-2 | 20 µg | $410.00 |
GHRHR encodes the growth hormone–releasing hormone receptor (GHRH-R), a class B GPCR expressed prominently in anterior pituitary somatotrophs where it binds hypothalamic GHRH to regulate growth hormone synthesis and secretion. Receptor activation primarily engages Gs–adenylyl cyclase signaling to elevate cAMP and activate PKA-dependent transcriptional programs, with additional coupling to MAPK and calcium-dependent pathways that influence endocrine cell proliferation and differentiation. Variation in GHRHR function is linked to dysregulated somatotropic axis activity and has been associated with growth hormone deficiency phenotypes and pituitary developmental abnormalities. In peripheral tissues and tumor models, GHRH/GHRHR signaling has also been used to study cAMP-driven transcription, cell-cycle control, and paracrine growth factor networks.
GHRH-R Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GHRHR locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GHRHR. 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 GHRHR 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 GHRHR-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.