Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
CRF-BP Double Nickase Plasmid (h): sc-403849-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CRF-BP 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-BP Double Nickase Plasmid (h) and CRF-BP Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting CRHBP. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CRF-BP Antibody (C-8): sc-365975
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CRF-BP Double Nickase Plasmid (h) | sc-403849-NIC | 20 µg | $410.00 | |||
CRF-BP Double Nickase Plasmid (h2) | sc-403849-NIC-2 | 20 µg | $410.00 |
CRHBP encodes corticotropin-releasing factor–binding protein (CRF-BP), a secreted glycoprotein that binds CRH and related urocortins to regulate ligand bioavailability and receptor engagement within the hypothalamic–pituitary–adrenal (HPA) axis. By buffering free CRH family peptides, CRF-BP modulates downstream CRHR1/CRHR2 signaling pathways that converge on cAMP/PKA and transcriptional programs controlling stress responsiveness, neuroendocrine secretion, and inflammatory tone. CRHBP expression is prominent in brain and peripheral tissues, where it can influence neuroimmune communication and endocrine homeostasis. Dysregulation of CRH–urocortin signaling and CRHBP expression patterns has been associated with stress-related neuropsychiatric phenotypes, altered metabolic regulation, and inflammatory processes, making it relevant for mechanistic studies of stress circuitry and peripheral CRF biology.
CRF-BP Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the CRHBP locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within CRHBP. 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 CRHBP 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 CRHBP-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.