
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TTYH1 CRISPR Activation Plasmid (h) | sc-408039-ACT | 20 µg | $397.00 |
TTYH1 (tweety family member 1) encodes a multi-pass membrane protein enriched in the nervous system and implicated in regulating ion homeostasis, membrane excitability, and cell volume dynamics. TTYH1 has been linked to processes such as calcium-activated signaling, chloride conductance–associated responses, and cytoskeletal remodeling that influence migration and neurite outgrowth. In cellular models, altered TTYH1 expression can affect proliferation and invasive behavior, consistent with reported associations to neurodevelopmental biology and brain tumor–related transcriptional programs. These features make TTYH1 a relevant node for studying membrane-associated signaling and microenvironmental adaptation pathways in human cells.
TTYH1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TTYH1 expression without altering the underlying DNA sequence.
TTYH1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TTYH1 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 TTYH1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TTYH1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TTYH1 locus and enabling the study of TTYH1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TTYH1 pathway restoration in tumor cells with silenced or reduced TTYH1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.