
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
A1 CRISPR Activation Plasmid (h) | sc-416421-ACT | 20 µg | $397.00 |
Human BCL2A1 encodes the anti-apoptotic BCL-2 family protein A1, a mitochondrial outer membrane regulator that preserves cell survival by sequestering BH3-only proteins and limiting BAX/BAK-mediated mitochondrial outer membrane permeabilization. A1 integrates signals from inflammatory and stress-responsive pathways, including NF-κB-dependent transcriptional programs, to modulate apoptosis, cell survival, and immune cell homeostasis. BCL2A1 expression is frequently inducible in hematopoietic lineages and can influence susceptibility to apoptotic cues during activation and differentiation. Dysregulated BCL2A1 activity and expression have been associated with altered apoptotic thresholding and survival phenotypes in cancer biology and inflammatory contexts, supporting mechanistic studies of cell fate control.
A1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BCL2A1 expression without altering the underlying DNA sequence.
A1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BCL2A1 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 BCL2A1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous A1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BCL2A1 locus and enabling the study of A1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of A1 pathway restoration in tumor cells with silenced or reduced BCL2A1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.