HIF1a Double Nickase Plasmid (m): sc-420856-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HIF1a Double Nickase Plasmid (m) 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
- HIF1a Double Nickase Plasmid (m) and HIF1a Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Hif1a. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: HIF1a Antibody (28b): sc-13515
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HIF1a Double Nickase Plasmid (m) | sc-420856-NIC | 20 µg | $410.00 | |||
HIF1a Double Nickase Plasmid (m2) | sc-420856-NIC-2 | 20 µg | $410.00 |
Mouse Hif1a encodes hypoxia-inducible factor 1 alpha (HIF1a), an oxygen-sensitive transcription factor that coordinates cellular adaptation to low oxygen tension. Under hypoxia, HIF1a escapes prolyl hydroxylase–VHL–mediated degradation, heterodimerizes with ARNT (HIF1β), and binds hypoxia response elements to reprogram transcription. This signaling axis regulates glycolytic metabolism, angiogenic and erythropoietic programs, iron handling, and cell survival, interfacing with PI3K–AKT–mTOR, MAPK, and mitochondrial stress pathways. Dysregulated HIF1a activity is widely studied in ischemia and inflammatory microenvironments and in models of tumor hypoxia where metabolic remodeling and altered immune signaling are key features.
HIF1a Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Hif1a locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Hif1a. 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 Hif1a 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 Hif1a-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.