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.
ChM-1 CRISPR Activation Plasmid (h): sc-403523-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ChM-1 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- ChM-1 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 ChM-1 CRISPR Activation Plasmid (h) and ChM-1 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the CNMD 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: ChM-1 Antibody (H-10): sc-365693
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ChM-1 CRISPR Activation Plasmid (h) | sc-403523-ACT | 20 µg | $397.00 |
CNMD encodes chondromodulin-1 (ChM-1), a secreted extracellular matrix-associated protein enriched in avascular cartilage and implicated in maintaining the anti-angiogenic microenvironment of developing and mature connective tissues. ChM-1 participates in regulation of endothelial cell behavior, cartilage homeostasis, and extracellular matrix remodeling, linking it to pathways that coordinate tissue vascularization and chondrogenic differentiation. Altered CNMD expression has been investigated in contexts of cartilage degeneration and aberrant neovascularization, where shifts in matrix signaling can influence inflammatory and hypoxic responses. As a result, CNMD is widely studied in musculoskeletal biology, vascular biology, and tumor microenvironment research as a modulator of stromal-vascular crosstalk.
ChM-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous CNMD expression without altering the underlying DNA sequence.
ChM-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the CNMD 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 CNMD transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ChM-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native CNMD locus and enabling the study of ChM-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ChM-1 pathway restoration in tumor cells with silenced or reduced CNMD expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.