
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DAD1 CRISPR Activation Plasmid (h) | sc-404172-ACT | 20 µg | $397.00 |
Human DAD1 (defender against apoptotic death 1) encodes an essential subunit of the oligosaccharyltransferase (OST) complex in the endoplasmic reticulum, where it supports N-linked glycosylation and proteostasis during co-translational protein maturation. By maintaining ER homeostasis, DAD1 influences unfolded protein response signaling and apoptosis susceptibility under cellular stress conditions. Altered DAD1 expression or function has been linked to dysregulated cell survival programs and glycoprotein-dependent processes relevant to oncogenic transformation and tissue degeneration. As a core component of the protein quality control network, DAD1 is frequently studied in pathways connecting ER stress, membrane protein biogenesis, and cell fate decisions.
DAD1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DAD1 expression without altering the underlying DNA sequence.
DAD1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DAD1 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 DAD1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DAD1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DAD1 locus and enabling the study of DAD1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DAD1 pathway restoration in tumor cells with silenced or reduced DAD1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.