PDE7B Lentiviral Activation Particles (h): sc-411961-LAC
- Target species: human
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- PDE7B 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
- PDE7B 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 PDE7B Lentiviral Activation Plasmid (h) and PDE7B Lentiviral Activation Plasmid (h2) target distinct regulatory regions of the PDE7B promoter. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PDE7B Lentiviral Activation Particles (h) | sc-411961-LAC | 200 µl | $455.00 |
Human PDE7B encodes phosphodiesterase 7B, a cAMP-specific enzyme that hydrolyzes cyclic AMP to 5′-AMP and thereby shapes the amplitude and duration of PKA- and EPAC-dependent signaling. By controlling intracellular cAMP pools, PDE7B influences transcriptional programs, cell survival, and differentiation across immune and nervous system contexts, intersecting with GPCR-driven signaling networks. Altered PDE7B expression or activity has been studied in relation to inflammatory signaling, neurotransmission, and hematologic and neurologic disease biology where cAMP homeostasis is a key regulatory node. PDE7B thus serves as a useful genetic handle for dissecting second-messenger signaling and pathway crosstalk in mechanistic cellular models.
PDE7B 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 PDE7B upregulation across a broader range of human cell types.
PDE7B 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 PDE7B transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PDE7B expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native PDE7B 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.