MOR-1 CRISPR Activation Plasmid (m): sc-422067-ACT

Oprm1 encodes the mouse μ-opioid receptor MOR-1, a Gi/Go-coupled GPCR that regulates neuronal excitability and synaptic transmission through inhibition of adenylyl cyclase, reduced cAMP/PKA signaling, modulation of ion channels, and engagement of MAPK pathways. MOR-1 is broadly expressed across pain, reward, and stress circuits where it integrates endogenous opioid peptide signals to shape analgesia, reinforcement, and affective behaviors. In immune and peripheral tissues, MOR-1 can influence neuroimmune crosstalk and inflammatory responses via GPCR-dependent signaling. Dysregulated Oprm1/MOR-1 signaling and genetic variation are frequently studied in contexts such as pain sensitivity, tolerance and dependence biology, substance use-related neuroadaptations, and stress-linked behavioral phenotypes in mouse models.

MOR-1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Oprm1 expression without altering the underlying DNA sequence.

MOR-1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Oprm1 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 Oprm1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MOR-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Oprm1 locus and enabling the study of MOR-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MOR-1 pathway restoration in tumor cells with silenced or reduced Oprm1 expression.

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