BTG1 Double Nickase Plasmid (h): sc-405339-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BTG1 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
- BTG1 Double Nickase Plasmid (h) and BTG1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BTG1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: BTG1 Antibody (2095C1a): sc-81207
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BTG1 Double Nickase Plasmid (h) | sc-405339-NIC | 20 µg | $410.00 |
BTG1 (B-cell translocation gene 1) encodes an antiproliferative protein in the TOB/BTG family that modulates cell-cycle progression, differentiation, and apoptosis through transcriptional and post-transcriptional control. BTG1 participates in pathways regulating mRNA deadenylation and turnover via interactions with CCR4–NOT components, and it can influence transcriptional programs linked to cellular quiescence and stress responses. In immune and hematopoietic contexts, BTG1 helps shape lymphocyte development and activation states, and altered BTG1 expression or disruption has been associated with dysregulated proliferation. Genetic lesions involving BTG1 have been reported in multiple lymphoid malignancy settings, supporting its relevance in studies of genome stability, oncogenic signaling, and lineage-specific growth control.
BTG1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BTG1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BTG1. 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 BTG1 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 BTG1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.