Olfr713 CRISPR Activation Plasmid (m): sc-435112-ACT

Olfr713 (mouse) encodes an olfactory receptor in the rhodopsin-like class A GPCR superfamily that contributes to odorant detection and chemosensory signal transduction in olfactory sensory neurons. Upon ligand engagement, olfactory receptors couple to heterotrimeric G proteins to regulate adenylyl cyclase activity, cAMP production, cyclic nucleotide–gated channel opening, and downstream neuronal depolarization. Olfr713 expression and function are relevant for studies of sensory neuron identity, receptor trafficking, and GPCR desensitization mechanisms that shape olfactory coding. Dysregulation of olfactory receptor pathways is frequently used as a systems-level readout in models of neuroinflammation, neurodegeneration, and environmental exposure, where altered chemosensory signaling can reflect broader changes in neuronal state.

Olfr713 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Olfr713 expression without altering the underlying DNA sequence.

Olfr713 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Olfr713 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 Olfr713 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Olfr713 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Olfr713 locus and enabling the study of Olfr713-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Olfr713 pathway restoration in tumor cells with silenced or reduced Olfr713 expression.

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