D1DR/Dopamine Receptor D1 CRISPR Activation Plasmid (h): sc-400532-ACT

DRD1 encodes the dopamine receptor D1 (D1DR), a G protein–coupled receptor that primarily couples to Gαs/olf to stimulate adenylyl cyclase, elevate intracellular cAMP, and activate PKA-dependent signaling cascades. In neurons, D1DR signaling modulates membrane excitability, synaptic plasticity, and gene expression programs through downstream effectors including CREB and DARPP-32, integrating dopaminergic tone with circuit-level function. DRD1 participates in dopamine-mediated pathways that shape reward, motivation, and motor control, and altered receptor expression or signaling dynamics are frequently investigated in neuropsychiatric and movement disorder research contexts. As a membrane receptor with tightly regulated expression, DRD1 is a useful target for studying GPCR desensitization, receptor trafficking, and crosstalk with other neuromodulatory systems.

D1DR/Dopamine Receptor D1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DRD1 expression without altering the underlying DNA sequence.

D1DR/Dopamine Receptor D1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DRD1 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 DRD1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous D1DR/Dopamine Receptor D1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DRD1 locus and enabling the study of D1DR/Dopamine Receptor D1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of D1DR/Dopamine Receptor D1 pathway restoration in tumor cells with silenced or reduced DRD1 expression.

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