
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BBS4 CRISPR Activation Plasmid (h) | sc-403421-ACT | 20 µg | $397.00 |
BBS4 encodes a core component of the BBSome, a multiprotein complex that mediates trafficking of membrane receptors and signaling proteins to and from the primary cilium. Through coordination of intraflagellar transport and ciliary membrane composition, BBS4 supports ciliogenesis and regulates cilia-dependent pathways including Hedgehog and other GPCR-linked signaling networks. Disruption of BBS4 perturbs ciliary signaling dynamics and cellular homeostasis in ciliated tissues. Variants in BBS4 are associated with Bardet–Biedl syndrome, linking altered ciliary transport to multisystem phenotypes relevant to neurodevelopmental, metabolic, and sensory biology research.
BBS4 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BBS4 expression without altering the underlying DNA sequence.
BBS4 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BBS4 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 BBS4 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BBS4 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BBS4 locus and enabling the study of BBS4-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BBS4 pathway restoration in tumor cells with silenced or reduced BBS4 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.