PDE4B Double Nickase Plasmid (m): sc-422161-NIC
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- PDE4B Double Nickase Plasmid (m) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- PDE4B Double Nickase Plasmid (m) and PDE4B Double Nickase Plasmid (m2) encode distinct paired gRNA designs targeting Pde4b. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PDE4B Double Nickase Plasmid (m) | sc-422161-NIC | 20 µg | $410.00 | |||
PDE4B Double Nickase Plasmid (m2) | sc-422161-NIC-2 | 20 µg | $410.00 |
Mouse Pde4b encodes phosphodiesterase 4B (PDE4B), a cAMP-specific phosphodiesterase that terminates signaling by hydrolyzing cyclic AMP to 5′-AMP. By shaping compartmentalized cAMP/PKA signaling, PDE4B influences phosphorylation programs that impact transcriptional outputs such as CREB-dependent gene expression, as well as cell-type-specific responses to GPCR activation. PDE4B activity is particularly relevant to immune and inflammatory signaling networks where cAMP levels modulate cytokine production, leukocyte activation, and signal integration downstream of receptors that elevate intracellular cAMP. Dysregulated PDE4B-dependent cAMP control has been associated with immune dysfunction and neurobehavioral phenotypes, making it a useful target for mechanistic studies in mouse cellular and in vivo models.
PDE4B Double Nickase Plasmid (m) consists of a matched pair of plasmids engineered for high-specificity editing of the Pde4b locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Pde4b. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt Pde4b function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of Pde4b-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.