
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
APLP1 CRISPR Activation Plasmid (h) | sc-403937-ACT | 20 µg | $397.00 |
Human APLP1 (amyloid beta precursor-like protein 1) is a type I transmembrane glycoprotein enriched in neurons and functionally related to the APP gene family. It contributes to synapse formation and maintenance, neurite outgrowth, and activity-dependent signaling, in part through regulated proteolysis and intracellular domain–mediated transcriptional effects. APLP1 participates in cell–cell adhesion processes and trafficking pathways that shape neuronal connectivity and synaptic plasticity. Dysregulated APP-family processing and synaptic dysfunction link APLP1-associated pathways to mechanisms studied in neurodegeneration and neurodevelopmental phenotypes, making it relevant for dissecting neuronal signaling networks.
APLP1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous APLP1 expression without altering the underlying DNA sequence.
APLP1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the APLP1 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 APLP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous APLP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native APLP1 locus and enabling the study of APLP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of APLP1 pathway restoration in tumor cells with silenced or reduced APLP1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.