Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
DDR2 CRISPR Activation Plasmid (h): sc-400414-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- DDR2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- DDR2 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by DDR2 CRISPR Activation Plasmid (h) and DDR2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the DDR2 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: DDR2 Antibody (3B11E4): sc-81707
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
DDR2 CRISPR Activation Plasmid (h) | sc-400414-ACT | 20 µg | $397.00 | |||
DDR2 CRISPR Activation Plasmid (h2) | sc-400414-ACT-2 | 20 µg | $397.00 |
Discoidin domain receptor 2 (DDR2) is a collagen-activated receptor tyrosine kinase that mediates cell–matrix signaling, regulating adhesion, migration, proliferation, and extracellular matrix remodeling. Upon binding fibrillar collagens, DDR2 triggers phosphorylation-dependent signaling through pathways such as MAPK/ERK, PI3K/AKT, and SRC family kinases, influencing cytoskeletal dynamics and transcriptional programs linked to tissue remodeling. DDR2 activity is implicated in stromal–tumor interactions and fibrotic processes through its role in collagen sensing and matrix turnover, and altered DDR2 signaling has been associated with changes in invasive behavior and mesenchymal phenotypes. These properties make DDR2 a useful target for studying collagen-driven signaling, EMT-like transitions, and microenvironmental regulation of cell fate.
DDR2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DDR2 expression without altering the underlying DNA sequence.
DDR2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DDR2 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 DDR2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous DDR2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DDR2 locus and enabling the study of DDR2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of DDR2 pathway restoration in tumor cells with silenced or reduced DDR2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.