
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PDE4B Lentiviral Activation Particles (m) | sc-422161-LAC | 200 µl | $455.00 |
Mouse Pde4b encodes the cAMP-specific phosphodiesterase PDE4B, a key regulator of intracellular second-messenger signaling that terminates cAMP responses by hydrolyzing cAMP to 5′-AMP. By shaping cAMP/PKA/CREB-dependent transcription and feedback to MAPK signaling, PDE4B influences receptor-driven signal integration and cellular activation thresholds. PDE4B activity contributes to modulation of inflammatory signaling networks, including pathways downstream of cytokine and Toll-like receptor stimulation, and is frequently studied in the context of immune cell function. Dysregulated PDE4B expression or signaling has been linked to inflammatory phenotypes and neuroimmune processes, supporting its use as a mechanistic node in disease-relevant pathway studies.
PDE4B Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Pde4b upregulation across a broader range of human cell types.
PDE4B Lentiviral Activation Particles (m) 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 Pde4b transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous PDE4B expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Pde4b 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.