
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BCAR3 CRISPR Activation Plasmid (h) | sc-404301-ACT | 20 µg | $397.00 | |||
BCAR3 CRISPR Activation Plasmid (h2) | sc-404301-ACT-2 | 20 µg | $397.00 |
BCAR3 (breast cancer anti-estrogen resistance 3) encodes an adaptor protein that couples receptor and integrin signaling to cytoskeletal remodeling and motility. BCAR3 interacts with CAS/BCAR1 and related focal adhesion components to modulate Src-family kinase activity, small GTPase signaling, and downstream pathways that influence cell adhesion, migration, and proliferation. Through these network connections, BCAR3 contributes to regulation of epithelial–mesenchymal dynamics and context-dependent growth signaling. Altered BCAR3 expression or signaling has been associated with tumor cell invasion and endocrine response phenotypes, making it a useful node for studying adhesion-driven oncogenic programs.
BCAR3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BCAR3 expression without altering the underlying DNA sequence.
BCAR3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BCAR3 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 BCAR3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BCAR3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BCAR3 locus and enabling the study of BCAR3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BCAR3 pathway restoration in tumor cells with silenced or reduced BCAR3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.