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.
HAS2 CRISPR Activation Plasmid (m): sc-420798-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- HAS2 CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- HAS2 CRISPR Activation Plasmid (m) 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 HAS2 CRISPR Activation Plasmid (m) and HAS2 CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Has2 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: HAS2 Antibody (A-7): sc-514737
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HAS2 CRISPR Activation Plasmid (m) | sc-420798-ACT | 20 µg | $397.00 |
Mouse Has2 encodes hyaluronan synthase 2 (HAS2), a plasma membrane enzyme that polymerizes hyaluronan, a major glycosaminoglycan of the extracellular matrix. HAS2-driven hyaluronan production modulates pericellular matrix organization, hydration, and mechanotransduction, influencing cell migration, adhesion, and proliferation through interactions with receptors such as CD44 and RHAMM. Regulation of Has2 links developmental morphogenesis and tissue remodeling to signaling networks including TGF-β, ERK/MAPK, and inflammatory cues that reshape extracellular matrix dynamics. Altered HAS2 activity and hyaluronan abundance are associated with fibrotic remodeling, vascular pathology, and tumor microenvironment biology, making Has2 a useful node for studying matrix-dependent phenotypes in vivo and in cultured mouse cells.
HAS2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Has2 expression without altering the underlying DNA sequence.
HAS2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Has2 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 Has2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous HAS2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Has2 locus and enabling the study of HAS2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of HAS2 pathway restoration in tumor cells with silenced or reduced Has2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.