
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α-tectorin CRISPR Activation Plasmid (h) | sc-405876-ACT | 20 µg | $397.00 |
TECTA encodes α-tectorin, a major non-collagenous glycoprotein of the inner ear tectorial membrane that helps organize extracellular matrix architecture required for efficient mechanoelectrical transduction by cochlear hair cells. Through its roles in matrix assembly and structural coupling between the tectorial membrane and stereocilia, α-tectorin supports sound-induced shearing forces and frequency tuning. Disruption of TECTA can perturb tectorial membrane integrity and alter auditory function, making it a key gene for studying sensory extracellular matrix biology. TECTA variation is associated with inherited forms of hearing impairment, linking α-tectorin function to disease-relevant phenotypes in auditory research models.
α-tectorin CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TECTA expression without altering the underlying DNA sequence.
α-tectorin CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TECTA 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 TECTA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous α-tectorin expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TECTA locus and enabling the study of α-tectorin-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of α-tectorin pathway restoration in tumor cells with silenced or reduced TECTA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.