P4HA1 Double Nickase Plasmid (h): sc-407173-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- P4HA1 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
- P4HA1 Double Nickase Plasmid (h) and P4HA1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting P4HA1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
P4HA1 Double Nickase Plasmid (h) | sc-407173-NIC | 20 µg | $410.00 | |||
P4HA1 Double Nickase Plasmid (h2) | sc-407173-NIC-2 | 20 µg | $410.00 |
P4HA1 encodes the catalytic alpha subunit of prolyl 4-hydroxylase, a key endoplasmic reticulum enzyme required for post-translational hydroxylation of proline residues in procollagen. This modification stabilizes the collagen triple helix and supports extracellular matrix maturation, influencing cell–matrix adhesion, migration, and tissue remodeling. P4HA1 activity links to oxygen- and redox-sensitive metabolic states that shape matrix deposition and proteostasis. Dysregulated P4HA1 expression is frequently studied in the context of fibrosis, tumor microenvironment remodeling, and other conditions characterized by altered collagen homeostasis.
P4HA1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the P4HA1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within P4HA1. 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 P4HA1 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 P4HA1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.