TSPAN7 CRISPR Activation Plasmid (h): sc-404065-ACT

Tetraspanin 7 (TSPAN7) is a four-pass transmembrane scaffold that organizes tetraspanin-enriched microdomains and coordinates the lateral assembly of cell-surface receptors, integrins, and signaling adaptors. In human cells, TSPAN7 influences membrane trafficking, actin cytoskeleton dynamics, and cell–cell communication processes that shape adhesion and motility programs, with notable roles in neuronal development and synaptic organization. Through these membrane-associated platforms, TSPAN7 can modulate receptor distribution and downstream signaling cascades linked to endocytosis and cytoskeletal remodeling. Altered TSPAN7 expression or function has been associated with neurodevelopmental phenotypes and has been investigated in contexts where membrane organization and signaling competence contribute to disease-relevant cellular states.

TSPAN7 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TSPAN7 expression without altering the underlying DNA sequence.

TSPAN7 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TSPAN7 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 TSPAN7 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TSPAN7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TSPAN7 locus and enabling the study of TSPAN7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TSPAN7 pathway restoration in tumor cells with silenced or reduced TSPAN7 expression.

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