
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
D54 CRISPR Activation Plasmid (h) | sc-407162-ACT | 20 µg | $397.00 |
Human TPD52L2 encodes D54, a member of the tumor protein D52-like family implicated in vesicle trafficking, membrane dynamics, and regulation of cell proliferation and survival programs. D54 has been linked to secretory and endocytic processes that can influence receptor recycling and intracellular signaling outputs, intersecting with pathways that coordinate growth and stress responses. Altered expression of TPD52L2 has been reported in multiple cancer and proliferative disease contexts, supporting its utility as a molecular handle for studying dysregulated cell state transitions. In basic research, D54 is used to probe mechanisms of intracellular transport coupled to oncogenic signaling and metabolic adaptation.
D54 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TPD52L2 expression without altering the underlying DNA sequence.
D54 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TPD52L2 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 TPD52L2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous D54 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TPD52L2 locus and enabling the study of D54-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of D54 pathway restoration in tumor cells with silenced or reduced TPD52L2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.