Olfr1261 CRISPR Activation Plasmid (m): sc-434614-ACT

Mouse Olfr1261 encodes an olfactory receptor in the rhodopsin-like class A GPCR family, typically functioning as a chemosensory detector that couples to G protein signaling to modulate cAMP-dependent pathways and downstream ion channel activity in olfactory neurons. Although olfactory receptors are enriched in the olfactory epithelium, many family members show ectopic expression, enabling studies of GPCR trafficking, membrane localization, and stimulus-dependent signal transduction in diverse cell contexts. Olfr1261 regulation can inform broader mechanisms of sensory receptor gene choice, neuronal differentiation, and chromatin-mediated control of large receptor gene clusters. Dysregulated GPCR signaling and altered chemosensory receptor expression patterns have been linked to changes in inflammation, metabolism, and tumor biology, supporting exploratory research into noncanonical olfactory receptor roles without implying clinical outcomes.

Olfr1261 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Olfr1261 expression without altering the underlying DNA sequence.

Olfr1261 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Olfr1261 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 Olfr1261 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Olfr1261 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Olfr1261 locus and enabling the study of Olfr1261-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Olfr1261 pathway restoration in tumor cells with silenced or reduced Olfr1261 expression.

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