
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Dab1 CRISPR Activation Plasmid (h) | sc-402167-ACT | 20 µg | $397.00 |
DAB1 encodes Disabled-1 (Dab1), a cytoplasmic adaptor protein that transduces Reelin signals to coordinate neuronal migration, cortical lamination, and neurite outgrowth during brain development. Upon Reelin engagement of VLDLR and LRP8 (ApoER2) receptors, Dab1 becomes tyrosine-phosphorylated and couples to downstream Src family kinases and cytoskeletal remodeling pathways that shape cell positioning and synaptic organization. This signaling axis intersects with actin dynamics, microtubule regulation, and protein turnover mechanisms that influence neuronal polarity and connectivity. Dysregulated DAB1/Reelin pathway activity is implicated in neurodevelopmental and neuropsychiatric disease biology, making DAB1 a useful node for mechanistic studies of brain circuit formation and cellular migration phenotypes.
Dab1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DAB1 expression without altering the underlying DNA sequence.
Dab1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DAB1 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 DAB1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Dab1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DAB1 locus and enabling the study of Dab1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Dab1 pathway restoration in tumor cells with silenced or reduced DAB1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.