
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BBS9 CRISPR Activation Plasmid (h) | sc-404329-ACT | 20 µg | $397.00 |
BBS9 encodes a core component of the BBSome complex that coordinates trafficking of membrane proteins to and from the primary cilium, supporting ciliary membrane composition and signal transduction fidelity. By partnering with other BBS proteins, BBS9 contributes to intraflagellar transport-associated processes that shape ciliogenesis and regulate receptor localization for pathways such as Hedgehog and other cilia-dependent signaling networks. Disruption of BBS9 function is linked to ciliopathy biology, where altered ciliary trafficking can impact developmental patterning, sensory signaling, and energy homeostasis. These features make BBS9 a useful target for probing cilium-dependent mechanisms, receptor transport dynamics, and genotype–phenotype relationships in human cellular models.
BBS9 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BBS9 expression without altering the underlying DNA sequence.
BBS9 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BBS9 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 BBS9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BBS9 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BBS9 locus and enabling the study of BBS9-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BBS9 pathway restoration in tumor cells with silenced or reduced BBS9 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.