
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DCC CRISPR Activation Plasmid (h) | sc-401035-ACT | 20 µg | $397.00 |
DCC (deleted in colorectal carcinoma) encodes a netrin-1 receptor and dependence receptor that coordinates axon guidance, neuronal migration, and cytoskeletal remodeling through cues in the extracellular matrix. In addition to developmental neurobiology, DCC signaling interfaces with pathways controlling cell adhesion, polarity, and apoptosis, with downstream effects on Rho GTPase dynamics and MAPK/PI3K-linked processes. Altered DCC expression or function has been associated with disrupted neural circuit formation and tumor biology, where changes in netrin–DCC signaling can influence survival signaling, invasion, and epithelial–mesenchymal-like behaviors. These features make human DCC a valuable target for studying guidance-cue transduction, cell–cell interactions, and context-dependent apoptotic responses.
DCC CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DCC expression without altering the underlying DNA sequence.
DCC CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DCC 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 DCC transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DCC expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DCC locus and enabling the study of DCC-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DCC pathway restoration in tumor cells with silenced or reduced DCC expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.