
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TP1 CRISPR Activation Plasmid (h) | sc-404178-ACT | 20 µg | $397.00 |
Human TEP1 encodes telomerase-associated protein 1 (TP1), a core component of telomerase and telomere maintenance machinery that supports chromosome end protection and long-term replicative capacity. TP1 contributes to telomerase RNP assembly/stability and links telomere biology to genome integrity pathways, including DNA damage signaling and cell cycle control. Dysregulation of telomerase-associated factors and telomere homeostasis is implicated in aging-related phenotypes and multiple disease contexts characterized by genomic instability. TEP1 is therefore studied in models of proliferative stress, senescence, and telomere-driven changes in transcriptional programs.
TP1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TEP1 expression without altering the underlying DNA sequence.
TP1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TEP1 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 TEP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TP1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TEP1 locus and enabling the study of TP1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TP1 pathway restoration in tumor cells with silenced or reduced TEP1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.