
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BACH1 Lentiviral Activation Particles (m) | sc-419283-LAC | 200 µl | $455.00 |
Mouse BACH1 (BTB and CNC homology 1) is a heme-responsive transcriptional repressor that heterodimerizes with small Maf proteins to regulate antioxidant and cytoprotective gene programs, including negative control of Hmox1. By integrating redox status with transcriptional output, BACH1 influences oxidative stress responses, iron/heme homeostasis, mitochondrial metabolism, and inflammatory signaling in multiple cell types. This regulatory axis is commonly studied in contexts where reactive oxygen species and stress-adaptive transcription shape cellular phenotypes, including models of chronic inflammation, fibrosis, metabolic dysfunction, and tumor-associated pathways.
BACH1 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Bach1 upregulation across a broader range of human cell types.
BACH1 Lentiviral Activation Particles (m) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the Bach1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous BACH1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Bach1 genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.