
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DcR2 CRISPR Activation Plasmid (h) | sc-403389-ACT | 20 µg | $397.00 |
TNFRSF10D encodes decoy receptor 2 (DcR2), a TNF receptor superfamily member that binds TRAIL (TNFSF10) but lacks a functional death domain, thereby attenuating extrinsic apoptotic signaling. By competing with death receptors such as DR4 (TNFRSF10A) and DR5 (TNFRSF10B), DcR2 can shift TRAIL pathway output toward survival-associated programs including NF-κB and MAPK signaling, influencing immune surveillance and cellular stress responses. Altered TNFRSF10D expression has been reported across multiple cancer contexts and is also linked to regulation of apoptosis resistance and senescence-associated phenotypes, making it relevant for studies of tumor biology, inflammation, and cell fate control.
DcR2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TNFRSF10D expression without altering the underlying DNA sequence.
DcR2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TNFRSF10D 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 TNFRSF10D transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DcR2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TNFRSF10D locus and enabling the study of DcR2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DcR2 pathway restoration in tumor cells with silenced or reduced TNFRSF10D expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.