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.
C1s CRISPR Activation Plasmid (h): sc-404794-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- C1s CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- C1s 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 C1s CRISPR Activation Plasmid (h) and C1s CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the C1S 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: C1s Antibody (D-6): sc-365273
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
C1s CRISPR Activation Plasmid (h) | sc-404794-ACT | 20 µg | $397.00 |
Human C1S encodes complement C1s, a serine protease that forms part of the C1 complex initiating the classical complement pathway. Upon activation, C1s cleaves C4 and C2 to generate the C3 convertase, driving opsonization, immune complex clearance, and downstream inflammatory signaling. Dysregulated C1s activity and complement activation are implicated in immune-mediated tissue injury and have been associated with autoimmune phenotypes, inflammatory disorders, and complement-driven pathology. C1S is therefore widely studied in innate immunity, serine protease regulation, and cross-talk between complement cascades and cellular stress responses.
C1s CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous C1S expression without altering the underlying DNA sequence.
C1s CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the C1S 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 C1S transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous C1s expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native C1S locus and enabling the study of C1s-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of C1s pathway restoration in tumor cells with silenced or reduced C1S expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.