Oxytocin-R CRISPR Activation Plasmid (h): sc-400641-ACT

Human OXTR encodes the oxytocin receptor (Oxytocin-R), a class A GPCR that couples primarily to Gq/11 to stimulate PLCβ-dependent IP3/DAG signaling, intracellular Ca²⁺ mobilization, and PKC activation. OXTR signaling influences MAPK/ERK and PI3K-AKT pathway crosstalk, shaping transcriptional programs that regulate smooth muscle contractility, social cognition, stress reactivity, and neuroendocrine communication. In peripheral tissues, OXTR contributes to uterine and mammary gland physiology, while in the CNS it modulates synaptic plasticity and circuit-level behaviors. Dysregulated OXTR expression or signaling has been associated with neuropsychiatric phenotypes, including autism spectrum-related traits, anxiety-related behaviors, and altered social attachment, supporting mechanistic studies in relevant cellular models.

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

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

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