Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
D2DR/Dopamine D2 Receptor Lentiviral Activation Particles (h): sc-400235-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- D2DR/Dopamine D2 Receptor Lentiviral Activation Particles (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- D2DR/Dopamine D2 Receptor Lentiviral Activation Particles (h) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
- Upon transduction, the SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by D2DR/Dopamine D2 Receptor Lentiviral Activation Plasmid (h) and D2DR/Dopamine D2 Receptor Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the DRD2 promoter. One or both designs may be available
- Following transfection, gene activation efficiency can be assayed by WB, IF or IHC using antibody: D2DR/Dopamine D2 Receptor Antibody (B-10): sc-5303
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
D2DR/Dopamine D2 Receptor Lentiviral Activation Particles (h) | sc-400235-LAC | 200 µl | $455.00 |
DRD2 encodes the human dopamine D2 receptor (D2DR), a Gi/o-coupled GPCR that modulates neurotransmission by inhibiting adenylyl cyclase, reducing cAMP/PKA signaling, and regulating ion channel activity. D2DR also engages β-arrestin–dependent signaling and kinase cascades such as ERK/MAPK and Akt/GSK3, shaping synaptic plasticity and neuronal excitability. Receptor signaling influences dopaminergic circuit function and presynaptic feedback control of dopamine release, with downstream effects on transcriptional programs and cellular metabolism. Altered DRD2 expression or signaling has been implicated in neuropsychiatric and neurodegenerative research contexts, supporting studies of receptor regulation, pathway bias, and network-level phenotypes.
D2DR/Dopamine D2 Receptor Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient DRD2 upregulation across a broader range of human cell types.
D2DR/Dopamine D2 Receptor Lentiviral Activation Particles (h) 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 DRD2 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous D2DR/Dopamine D2 Receptor expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native DRD2 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.