TTP-α CRISPR Activation Plasmid (h): sc-411045-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- TTP-α CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- TTP-α 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 TTP-α CRISPR Activation Plasmid (h) and TTP-α CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the TTPA transcriptional start site. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TTP-α CRISPR Activation Plasmid (h) | sc-411045-ACT | 20 µg | $397.00 |
TTPA encodes α‑tocopherol transfer protein (TTP‑α), a cytosolic lipid-binding protein that selectively traffics α‑tocopherol (vitamin E) to support cellular antioxidant defense and membrane integrity. By governing intracellular vitamin E distribution, TTP‑α influences redox homeostasis, lipid peroxidation susceptibility, and stress-responsive signaling linked to mitochondrial and endoplasmic reticulum function. Altered TTPA activity is associated with neurodegenerative phenotypes and oxidative stress–related tissue vulnerability, reflecting the importance of α‑tocopherol handling in long-lived, metabolically active cells. Human TTPA regulation is therefore relevant to studies of lipid metabolism, oxidative injury, and genotype–phenotype relationships in neuronal and hepatic models.
TTP-α CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TTPA expression without altering the underlying DNA sequence.
TTP-α CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TTPA 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 TTPA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TTP-α expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TTPA locus and enabling the study of TTP-α-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TTP-α pathway restoration in tumor cells with silenced or reduced TTPA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.