
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TREML2 CRISPR Activation Plasmid (m) | sc-435918-ACT | 20 µg | $397.00 |
Treml2 encodes triggering receptor expressed on myeloid cells-like 2 (TREML2), a type I membrane receptor enriched in myeloid-lineage cells and implicated in innate immune sensing and inflammatory signaling. TREML2 has been linked to modulation of microglial and macrophage activation states, shaping cytokine production, phagocytic responses, and cross-talk with adaptive immunity. Through these processes, Treml2 is frequently studied in pathways governing neuroinflammation and tissue-resident myeloid homeostasis, with relevance to models of neurodegeneration, autoimmune inflammation, and infection. Its cell-surface localization and context-dependent expression make it a useful node for dissecting receptor-mediated immune regulation in mouse systems.
TREML2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Treml2 expression without altering the underlying DNA sequence.
TREML2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Treml2 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 Treml2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TREML2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Treml2 locus and enabling the study of TREML2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TREML2 pathway restoration in tumor cells with silenced or reduced Treml2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.