Tescalcin Lentiviral Activation Particles (h): sc-408244-LAC

Human TESC encodes tescalcin, a small EF-hand Ca²⁺-binding protein enriched in hematopoietic and excitable cell contexts that acts as a calcium-dependent regulator of signaling and cellular differentiation programs. Tescalcin interacts with select partners to modulate kinase/phosphatase balance and Ca²⁺-linked pathways, influencing processes such as proliferation, lineage commitment, and stimulus-responsive transcriptional outputs. Through its sensitivity to intracellular calcium dynamics, tescalcin can impact MAPK-associated signaling and other downstream networks that couple calcium flux to changes in gene expression and cell state. Altered TESC expression has been reported in multiple disease-relevant settings, supporting its utility as a mechanistic node for studying dysregulated signaling, differentiation, and cellular stress responses.

Tescalcin Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient TESC upregulation across a broader range of human cell types.

Tescalcin Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the TESC transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Tescalcin expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TESC genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

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