DSCAM CRISPR Activation Plasmid (h): sc-403385-ACT

DSCAM (Down syndrome cell adhesion molecule) encodes an immunoglobulin superfamily cell-surface receptor that mediates cell–cell recognition and neurite guidance, supporting axon pathfinding, dendritic self-avoidance, and synaptic connectivity during human nervous system development. DSCAM signaling interfaces with adhesion-dependent cytoskeletal remodeling and kinase pathways that influence neurite outgrowth, including SRC-family signaling and downstream actin dynamics. Altered DSCAM dosage or regulation has been associated with neurodevelopmental phenotypes, including conditions linked to copy-number changes and trisomy-related gene dosage imbalance. As a model for contact-dependent wiring specificity, DSCAM is widely studied in neuronal differentiation, circuit assembly, and cell adhesion biology.

DSCAM CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DSCAM expression without altering the underlying DNA sequence.

DSCAM CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DSCAM 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 DSCAM transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DSCAM expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DSCAM locus and enabling the study of DSCAM-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DSCAM pathway restoration in tumor cells with silenced or reduced DSCAM expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.