DSCAML1 CRISPR Activation Plasmid (h): sc-409552-ACT

DSCAML1 (Down syndrome cell adhesion molecule-like 1) encodes a neuronal immunoglobulin superfamily cell-adhesion receptor implicated in neurite outgrowth, axon guidance, and synapse organization during neurodevelopment. Through homophilic and heterophilic interactions at the cell surface, DSCAML1 contributes to contact-dependent signaling that shapes neural circuit assembly and dendritic patterning. Dysregulated DSCAML1 expression or variation has been associated with neurodevelopmental and neuropsychiatric phenotypes, supporting its relevance for studies of synaptic connectivity and brain development. In human cell models, DSCAML1 provides a tractable node for probing adhesion-dependent pathways that coordinate neuronal differentiation and network formation.

DSCAML1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DSCAML1 expression without altering the underlying DNA sequence.

DSCAML1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DSCAML1 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 DSCAML1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DSCAML1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DSCAML1 locus and enabling the study of DSCAML1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DSCAML1 pathway restoration in tumor cells with silenced or reduced DSCAML1 expression.

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