Olfr303 CRISPR Activation Plasmid (m): sc-434741-ACT

Olfr303 encodes a mouse olfactory receptor in the class A rhodopsin-like GPCR superfamily, typically expressed in olfactory sensory neurons where it contributes to odorant detection and signal transduction. Upon ligand engagement, olfactory receptors couple to G protein–mediated pathways that promote cAMP production, cyclic nucleotide–gated channel activity, membrane depolarization, and downstream transcriptional programs involved in neuronal activity and sensory adaptation. Beyond olfaction, ectopic expression of olfactory receptors has been reported across diverse tissues, motivating studies of GPCR-linked regulation of cell signaling, differentiation, and microenvironmental sensing. Dysregulated GPCR signaling is broadly relevant to neurobiology and cancer biology, making Olfr303 a useful model for interrogating receptor-driven signaling states in mouse systems.

Olfr303 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Olfr303 expression without altering the underlying DNA sequence.

Olfr303 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Olfr303 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 Olfr303 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Olfr303 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Olfr303 locus and enabling the study of Olfr303-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Olfr303 pathway restoration in tumor cells with silenced or reduced Olfr303 expression.

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