
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RPGRIP1L CRISPR Activation Plasmid (h) | sc-404458-ACT | 20 µg | $397.00 |
RPGRIP1L encodes a ciliary transition zone protein that scaffolds RPGR-interacting components and helps establish the diffusion barrier controlling protein trafficking into and out of the primary cilium. It participates in centrosome/basal body organization and supports Hedgehog and other cilia-dependent signaling pathways that coordinate embryonic patterning and tissue homeostasis. Disruption of RPGRIP1L perturbs ciliogenesis and signal transduction, linking altered ciliary gating to pleiotropic developmental phenotypes. Genetic variation in RPGRIP1L has been associated with ciliopathies, including Joubert and Meckel spectrum disorders, making it a useful node for studying cilia-driven disease mechanisms in human cells.
RPGRIP1L CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RPGRIP1L expression without altering the underlying DNA sequence.
RPGRIP1L CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RPGRIP1L 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 RPGRIP1L transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous RPGRIP1L expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RPGRIP1L locus and enabling the study of RPGRIP1L-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of RPGRIP1L pathway restoration in tumor cells with silenced or reduced RPGRIP1L expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.