
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BACH2 CRISPR Activation Plasmid (m) | sc-419284-ACT | 20 µg | $397.00 |
Bach2 encodes the BTB/POZ and CNC homology transcription factor BACH2, a key regulator of gene expression programs that balance immune activation with tolerance. In mouse, BACH2 shapes lymphocyte development and function, including B cell maturation, class-switch–associated transcriptional networks, and T cell lineage decisions such as regulatory T cell stability and effector differentiation. It integrates signaling and chromatin-associated processes to modulate cytokine responses, oxidative stress pathways, and apoptosis-related checkpoints. Dysregulated BACH2 activity is associated with immune-mediated pathology and altered lymphoid homeostasis, supporting its use in mechanistic studies of autoimmunity, inflammation, and hematologic disease models.
BACH2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Bach2 expression without altering the underlying DNA sequence.
BACH2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Bach2 locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the Bach2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BACH2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Bach2 locus and enabling the study of BACH2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BACH2 pathway restoration in tumor cells with silenced or reduced Bach2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.