
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TPCN1 CRISPR Activation Plasmid (h) | sc-404943-ACT | 20 µg | $397.00 |
Human TPCN1 (two-pore channel 1) encodes an endolysosomal cation channel that regulates NAADP-sensitive Ca2+ release from acidic organelles, coordinating intracellular calcium microdomains with membrane trafficking. By shaping endosome–lysosome dynamics, vesicular fusion, and organelle excitability, TPCN1 influences autophagy, receptor recycling, and signaling pathways linked to cellular metabolism and stress responses. Altered endolysosomal Ca2+ handling and trafficking phenotypes associated with TPCN1 activity are relevant to investigations of neurodegeneration, cardiometabolic dysfunction, and host–pathogen entry mechanisms. As a result, TPCN1 is frequently studied in models that connect lysosomal function to Ca2+-dependent signal transduction and proteostasis.
TPCN1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TPCN1 expression without altering the underlying DNA sequence.
TPCN1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TPCN1 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 TPCN1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TPCN1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TPCN1 locus and enabling the study of TPCN1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TPCN1 pathway restoration in tumor cells with silenced or reduced TPCN1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.