
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LYSMD3 CRISPR Activation Plasmid (h) | sc-409014-ACT | 20 µg | $397.00 |
Human LYSMD3 encodes a LysM domain–containing membrane-associated protein implicated in innate immune sensing at mucosal and epithelial interfaces. LysM motifs commonly mediate binding to carbohydrate-containing microbial structures, linking LYSMD3 to pattern-recognition signaling and modulation of inflammatory responses in myeloid and barrier cell types. Perturbation of such sensing pathways can influence cytokine programs, epithelial defense, and interactions with the microbiome. Accordingly, LYSMD3 is of interest in studies of inflammatory signaling networks and disease contexts where dysregulated innate immunity contributes to pathology.
LYSMD3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LYSMD3 expression without altering the underlying DNA sequence.
LYSMD3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LYSMD3 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 LYSMD3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous LYSMD3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LYSMD3 locus and enabling the study of LYSMD3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of LYSMD3 pathway restoration in tumor cells with silenced or reduced LYSMD3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.