
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BAI-1 CRISPR Activation Plasmid (m) | sc-430764-ACT | 20 µg | $397.00 |
Mouse Adgrb1 encodes brain-specific angiogenesis inhibitor 1 (BAI-1), an adhesion GPCR enriched in the nervous system and vascular-associated microenvironments. BAI-1 participates in cell–cell and cell–matrix interactions, promotes recognition of apoptotic cells via phosphatidylserine-dependent engulfment, and modulates cytoskeletal remodeling through Rho-family GTPase signaling. Proteolytic processing can release anti-angiogenic fragments, linking BAI-1 to regulation of vascular growth and tissue homeostasis. Altered BAI-1 expression or function has been implicated in pathways relevant to neuroinflammation, synaptic organization, tumor microenvironment biology, and aberrant angiogenesis, making it a useful node for mechanistic studies of CNS and vascular phenotypes.
BAI-1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Adgrb1 expression without altering the underlying DNA sequence.
BAI-1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Adgrb1 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 Adgrb1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BAI-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Adgrb1 locus and enabling the study of BAI-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BAI-1 pathway restoration in tumor cells with silenced or reduced Adgrb1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.