SNX9 CRISPR Activation Plasmid (h): sc-403578-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SNX9 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- SNX9 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 SNX9 CRISPR Activation Plasmid (h) and SNX9 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SNX9 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: SNX9 Antibody (G-5): sc-166863
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SNX9 CRISPR Activation Plasmid (h) | sc-403578-ACT | 20 µg | $397.00 |
Human SNX9 (sorting nexin 9) is a PX-BAR domain adaptor that links phosphoinositide recognition to membrane remodeling and actin dynamics. It functions at clathrin-mediated endocytosis by coordinating AP-2/clathrin components with dynamin-dependent vesicle scission and by coupling endocytic sites to Arp2/3-driven actin polymerization through interactions with N-WASP and related factors. Through these roles, SNX9 contributes to receptor internalization, trafficking, and signal attenuation, influencing pathways such as EGFR and other RTK-linked signaling networks. Altered SNX9 expression or function has been associated with dysregulated vesicle trafficking and signaling states observed in cancer and neurobiological disease contexts, making it a useful node for mechanistic studies of endocytosis-linked signaling.
SNX9 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SNX9 expression without altering the underlying DNA sequence.
SNX9 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SNX9 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 SNX9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SNX9 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SNX9 locus and enabling the study of SNX9-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SNX9 pathway restoration in tumor cells with silenced or reduced SNX9 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.