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.
Paraxis CRISPR Activation Plasmid (h): sc-403926-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Paraxis CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Paraxis 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 Paraxis CRISPR Activation Plasmid (h) and Paraxis CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the TCF15 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: Paraxis Antibody (B-6): sc-514687
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Paraxis CRISPR Activation Plasmid (h) | sc-403926-ACT | 20 µg | $397.00 |
Human TCF15 encodes Paraxis, a basic helix–loop–helix transcription factor that orchestrates paraxial mesoderm patterning and somite compartmentalization during embryogenesis. Paraxis regulates lineage programs that govern myogenic and chondrogenic differentiation, coordinating transcriptional networks involved in epithelialization, cell fate commitment, and tissue morphogenesis. Through its role in developmental gene regulation, TCF15 is studied in pathways that shape musculoskeletal formation and in models of aberrant differentiation states relevant to congenital developmental defects and cancer-associated transcriptional reprogramming. Dysregulated TCF15 expression has been reported in multiple tumor contexts, motivating its use as a node for dissecting context-specific transcriptional control and cell identity transitions.
Paraxis CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TCF15 expression without altering the underlying DNA sequence.
Paraxis CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TCF15 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 TCF15 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Paraxis expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TCF15 locus and enabling the study of Paraxis-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Paraxis pathway restoration in tumor cells with silenced or reduced TCF15 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.