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.
aggrecan CRISPR Activation Plasmid (h): sc-400760-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- aggrecan CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- aggrecan 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 aggrecan CRISPR Activation Plasmid (h) and aggrecan CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the ACAN 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: aggrecan Antibody (4F4): sc-33695
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
aggrecan CRISPR Activation Plasmid (h) | sc-400760-ACT | 20 µg | $397.00 | |||
aggrecan CRISPR Activation Plasmid (h2) | sc-400760-ACT-2 | 20 µg | $397.00 |
ACAN encodes aggrecan, a large chondroitin sulfate proteoglycan that is a principal structural component of cartilage extracellular matrix. Aggrecan interacts with hyaluronan and link protein to form high–molecular weight aggregates that provide osmotic swelling pressure and load-bearing resilience in articular cartilage, influencing chondrocyte mechanotransduction and matrix homeostasis. ACAN expression and turnover are tightly coupled to extracellular matrix organization, glycosaminoglycan biosynthesis, and proteolytic remodeling by aggrecanases such as ADAMTS family members. Dysregulated aggrecan synthesis or accelerated cleavage is associated with cartilage degeneration and altered skeletal development, making ACAN a key gene for studying chondrocyte biology and matrix catabolism.
aggrecan CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ACAN expression without altering the underlying DNA sequence.
aggrecan CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ACAN 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 ACAN transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous aggrecan expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ACAN locus and enabling the study of aggrecan-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of aggrecan pathway restoration in tumor cells with silenced or reduced ACAN expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.