TRF1 Double Nickase Plasmid (m): sc-423339-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TRF1 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
- TRF1 Double Nickase Plasmid (m) and TRF1 Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Terf1. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRF1 Double Nickase Plasmid (m) | sc-423339-NIC | 20 µg | $410.00 | |||
TRF1 Double Nickase Plasmid (m2) | sc-423339-NIC-2 | 20 µg | $410.00 |
Mouse Terf1 encodes TRF1, a core component of the shelterin complex that binds double-stranded telomeric repeats to regulate telomere length and architecture. TRF1 modulates telomeric replication dynamics, suppresses aberrant DNA damage signaling at chromosome ends, and coordinates with replication and repair factors to maintain genome stability. Through its roles in telomere capping and replication, TRF1 influences pathways linked to cell-cycle control, senescence, and chromosomal instability. Dysregulated TRF1 function or telomere maintenance is broadly associated with age-related decline and cancer-relevant genome instability phenotypes in research models.
TRF1 Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Terf1 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Terf1. 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 Terf1 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 Terf1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.