
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FAIM2 CRISPR Activation Plasmid (h) | sc-404103-ACT | 20 µg | $397.00 |
FAIM2 (Fas apoptotic inhibitory molecule 2), also known as Lifeguard, is a membrane-associated anti-apoptotic protein that modulates death receptor signaling and neuronal survival. It attenuates Fas/CD95-mediated apoptosis, influencing extrinsic apoptotic cascades, caspase activation, and stress-response pathways that govern cell fate decisions. FAIM2 expression is enriched in neural tissues and has been linked to mechanisms of neuroprotection, synaptic maintenance, and cellular resilience under inflammatory or metabolic stress. Dysregulated FAIM2 activity has been associated with altered susceptibility to apoptosis in contexts relevant to neurodegeneration, metabolic phenotypes, and tumor cell survival biology.
FAIM2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FAIM2 expression without altering the underlying DNA sequence.
FAIM2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FAIM2 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 FAIM2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FAIM2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FAIM2 locus and enabling the study of FAIM2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FAIM2 pathway restoration in tumor cells with silenced or reduced FAIM2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.