Tescalcin CRISPR Activation Plasmid (h): sc-408244-ACT

Human TESC encodes tescalcin, a Ca2+-binding protein with an EF-hand motif that functions as a signaling modulator in the cytosol and at membranes. Tescalcin has been implicated in coupling calcium flux to protein–protein interaction networks that influence MAPK/ERK signaling, ion transporter regulation, and cellular differentiation programs, particularly in hematopoietic lineages. Through these pathways, TESC can affect proliferation, migration, and lineage commitment in a context-dependent manner. Altered TESC expression has been reported in cancer-relevant transcriptional states and differentiation-associated phenotypes, making it useful for mechanistic studies of calcium-dependent signaling and gene regulatory networks.

Tescalcin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TESC expression without altering the underlying DNA sequence.

Tescalcin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TESC 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 TESC transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Tescalcin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TESC locus and enabling the study of Tescalcin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Tescalcin pathway restoration in tumor cells with silenced or reduced TESC expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.