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.
SRp30c CRISPR Activation Plasmid (h): sc-403790-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- SRp30c CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- SRp30c 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 SRp30c CRISPR Activation Plasmid (h) and SRp30c CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the SRSF9 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: SRp30c Antibody (1G7): sc-293314
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SRp30c CRISPR Activation Plasmid (h) | sc-403790-ACT | 20 µg | $397.00 |
SRSF9 encodes the human serine/arginine-rich splicing factor SRp30c, an RNA-binding protein that regulates constitutive and alternative pre-mRNA splicing and contributes to exon definition. SRp30c influences transcript isoform output and RNA processing decisions that intersect with spliceosome assembly, mRNA export, and broader gene expression programs. Altered activity or expression of SR family splicing regulators can shift isoform balance across cell-cycle, stress-response, and differentiation networks, linking splicing dysregulation to disease-associated transcriptional states. Consequently, SRSF9 is commonly studied for its role in post-transcriptional control and for mapping splicing-dependent regulatory pathways in human cells.
SRp30c CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SRSF9 expression without altering the underlying DNA sequence.
SRp30c CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SRSF9 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 SRSF9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SRp30c expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SRSF9 locus and enabling the study of SRp30c-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SRp30c pathway restoration in tumor cells with silenced or reduced SRSF9 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.