
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TRPC7 CRISPR Activation Plasmid (h) | sc-403911-ACT | 20 µg | $397.00 |
TRPC7 encodes a calcium-permeable, nonselective cation channel in the transient receptor potential canonical (TRPC) family that contributes to receptor-operated Ca2+ entry following PLC-coupled receptor signaling and diacylglycerol production. By shaping intracellular Ca2+ dynamics, TRPC7 influences membrane depolarization and downstream signaling nodes such as CaM-dependent pathways, MAPK cascades, and NFAT-driven transcriptional programs. TRPC7 activity has been linked to regulation of cellular excitability, secretion, and cytoskeletal remodeling across diverse cell types. Altered TRP channel signaling, including TRPC family dysregulation, is frequently studied in the context of aberrant calcium homeostasis relevant to cardiovascular, neurological, and proliferative disease phenotypes.
TRPC7 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TRPC7 expression without altering the underlying DNA sequence.
TRPC7 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TRPC7 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 TRPC7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TRPC7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TRPC7 locus and enabling the study of TRPC7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TRPC7 pathway restoration in tumor cells with silenced or reduced TRPC7 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.