
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRPC1 CRISPR Activation Plasmid (h) | sc-401040-ACT | 20 µg | $397.00 |
TRPC1 encodes a canonical transient receptor potential channel subunit that contributes to receptor-operated and store-operated Ca²⁺ entry, shaping cytosolic calcium signals that regulate proliferation, migration, secretion, and cytoskeletal remodeling. TRPC1 activity integrates with PLC/IP₃ signaling and calcium-dependent effectors such as calmodulin and calcineurin/NFAT to modulate transcriptional and metabolic programs. Altered TRPC1 expression or channel function has been associated with dysregulated calcium homeostasis observed across cardiovascular, neuromuscular, and cancer-related cellular phenotypes. As a widely expressed membrane protein, TRPC1 is frequently studied in models of mechanosensation, oxidative stress responses, and epithelial-to-mesenchymal transition–linked processes.
TRPC1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TRPC1 expression without altering the underlying DNA sequence.
TRPC1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TRPC1 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 TRPC1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TRPC1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TRPC1 locus and enabling the study of TRPC1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TRPC1 pathway restoration in tumor cells with silenced or reduced TRPC1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.