RTP1 CRISPR Activation Plasmid (m): sc-433714-ACT

Mouse Rtp1 encodes receptor transporter protein 1 (RTP1), a membrane-associated accessory factor that promotes endoplasmic reticulum processing, trafficking, and functional surface expression of odorant receptors in olfactory sensory neurons. By facilitating receptor maturation and export through the secretory pathway, RTP1 influences GPCR signaling competence and odor-evoked sensory transduction. Rtp1 expression is closely tied to neuronal differentiation programs within the olfactory epithelium and can shape receptor repertoire functionality at the cell surface. Dysregulation of receptor trafficking machinery such as RTP1 is relevant to studies of sensory dysfunction, neuronal stress responses, and GPCR biogenesis in neurobiology.

RTP1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Rtp1 expression without altering the underlying DNA sequence.

RTP1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Rtp1 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 Rtp1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous RTP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Rtp1 locus and enabling the study of RTP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of RTP1 pathway restoration in tumor cells with silenced or reduced Rtp1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.