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.
Jagged1 CRISPR Activation Plasmid (h): sc-400208-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Jagged1 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Jagged1 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 Jagged1 CRISPR Activation Plasmid (h) and Jagged1 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the JAG1 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: Jagged1 Antibody (E-12): sc-390177
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Jagged1 CRISPR Activation Plasmid (h) | sc-400208-ACT | 20 µg | $397.00 | |||
Jagged1 CRISPR Activation Plasmid (h2) | sc-400208-ACT-2 | 20 µg | $397.00 |
Human JAG1 encodes Jagged1, a membrane-bound ligand that activates canonical Notch signaling through receptor engagement on adjacent cells, promoting proteolytic release of the Notch intracellular domain and transcriptional reprogramming. This pathway regulates cell fate specification, differentiation, stem and progenitor cell maintenance, and tissue patterning during development and in adult homeostasis. Jagged1-driven Notch activity integrates with angiogenic, inflammatory, and extracellular matrix remodeling programs to shape microenvironmental cues and intercellular communication. Dysregulated JAG1/Notch signaling has been associated with developmental disorders and diverse pathologies, including oncogenic processes and vascular abnormalities, making it a frequent target in mechanistic pathway studies.
Jagged1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous JAG1 expression without altering the underlying DNA sequence.
Jagged1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the JAG1 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 JAG1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Jagged1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native JAG1 locus and enabling the study of Jagged1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Jagged1 pathway restoration in tumor cells with silenced or reduced JAG1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.