
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Olfr666 Lentiviral Activation Particles (m) | sc-435166-LAC | 200 µl | $455.00 |
Olfr666 encodes an olfactory receptor in mouse, part of the large G protein–coupled receptor (GPCR) superfamily that detects odorant ligands and initiates sensory signal transduction. Upon activation, olfactory receptors typically couple to G proteins to stimulate adenylyl cyclase, elevate cAMP, and gate cyclic nucleotide–dependent ion channels, converting chemical cues into neuronal activity. Although classically associated with olfactory sensory neurons, ectopic expression of some olfactory receptors has been reported in non-olfactory tissues, motivating studies of GPCR signaling beyond smell. Dysregulation of GPCR-mediated pathways is broadly relevant to neurobiology and cellular homeostasis, providing a rationale for interrogating Olfr666 expression and function in sensory and signaling models.
Olfr666 Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Olfr666 upregulation across a broader range of human cell types.
Olfr666 Lentiviral Activation Particles (m) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the Olfr666 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Olfr666 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Olfr666 genomic locus and regulatory architecture.
The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.