
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CRX CRISPR Activation Plasmid (h) | sc-401736-ACT | 20 µg | $397.00 |
CRX (cone-rod homeobox) encodes a photoreceptor-specific homeodomain transcription factor that orchestrates retinal development and the maintenance of rod and cone identity. In the nucleus, CRX binds cis-regulatory elements to control transcriptional programs governing phototransduction, outer segment biogenesis, and synaptic function, acting in concert with other retinal regulators such as NRL and OTX2. Tight regulation of CRX-dependent gene networks is essential for photoreceptor survival and visual function. Genetic perturbations in CRX and its downstream targets are associated with inherited retinal degenerations, including retinitis pigmentosa, cone-rod dystrophy, and Leber congenital amaurosis, making CRX a key node for mechanistic studies of retinal gene regulation.
CRX CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CRX expression without altering the underlying DNA sequence.
CRX CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CRX 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 CRX transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CRX expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CRX locus and enabling the study of CRX-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CRX pathway restoration in tumor cells with silenced or reduced CRX expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.