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.
BACH1 Double Nickase Plasmid (h): sc-401047-NIC
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BACH1 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
- BACH1 Double Nickase Plasmid (h) and BACH1 Double Nickase Plasmid (h2) encode distinct paired gRNA designs targeting BACH1. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: BACH1 Antibody (F-9): sc-271211
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BACH1 Double Nickase Plasmid (h) | sc-401047-NIC | 20 µg | $410.00 | |||
BACH1 Double Nickase Plasmid (h2) | sc-401047-NIC-2 | 20 µg | $410.00 |
BACH1 (BTB and CNC homology 1) encodes a heme-responsive transcription factor that heterodimerizes with small MAF proteins to repress antioxidant response element (ARE)-driven genes, including components of heme catabolism and oxidative stress defense. By integrating heme availability with redox homeostasis, BACH1 modulates mitochondrial function, iron metabolism, and cellular responses to reactive oxygen species, intersecting with NRF2/KEAP1 signaling and stress-adaptive transcriptional programs. Dysregulated BACH1 activity has been linked to altered oxidative stress tolerance, inflammatory signaling, and changes in proliferation and differentiation states across multiple disease-relevant cellular contexts. These properties make BACH1 a useful node for mechanistic studies of redox-regulated transcription, metabolic adaptation, and stress-induced gene networks.
BACH1 Double Nickase Plasmid (h) consists of a matched pair of plasmids engineered for high-specificity editing of the BACH1 locus in human cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within BACH1. 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 BACH1 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 BACH1-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.