GHRH Double Nickase Plasmid (h): sc-404753-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GHRH 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 Double Nickase Plasmid (h) and GHRH Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting GHRH. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GHRH Double Nickase Plasmid (h) | sc-404753-NIC | 20 µg | $410.00 | |||
GHRH Double Nickase Plasmid (h2) | sc-404753-NIC-2 | 20 µg | $410.00 |
Human GHRH encodes growth hormone–releasing hormone, a hypothalamic neuropeptide that binds GHRHR on pituitary somatotrophs to stimulate growth hormone synthesis and secretion. Through cAMP/PKA signaling, GHRH regulates pulsatile GH release and influences downstream IGF-1 axis activity, linking neuroendocrine control to systemic growth, metabolism, and tissue homeostasis. GHRH signaling intersects with pathways governing energy balance, sleep and circadian neurobiology, and stress-responsive endocrine regulation. Dysregulation of the GHRH–GHRHR–GH axis is relevant to disorders of growth and metabolic phenotype and provides a mechanistic entry point for studying neuroendocrine contributions to pituitary function and hormone-driven physiology.
GHRH Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the GHRH locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within GHRH. 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 GHRH 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 GHRH-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.