
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TICAM-1 CRISPR Activation Plasmid (h) | sc-414627-ACT | 20 µg | $397.00 |
TICAM1 encodes TICAM-1 (also known as TRIF), an essential adaptor in innate immune signaling downstream of TLR3 and TLR4 that links pattern-recognition receptor activation to IRF3/IRF7- and NF-κB-dependent transcriptional programs. Through recruitment of TBK1 and IKKε and integration with TRAF/RIPK1 signaling nodes, TICAM-1 coordinates type I interferon production, inflammatory cytokine induction, and programmed cell death pathways. Dysregulated TICAM1 signaling has been associated with altered antiviral responses and aberrant inflammation, and it is frequently examined in the context of immune-mediated and infectious disease biology. As a result, TICAM1 is widely used as a mechanistic handle to probe TLR-dependent innate immune pathways and their crosstalk with cell stress and cytokine networks.
TICAM-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TICAM1 expression without altering the underlying DNA sequence.
TICAM-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TICAM1 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 TICAM1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TICAM-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TICAM1 locus and enabling the study of TICAM-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TICAM-1 pathway restoration in tumor cells with silenced or reduced TICAM1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.