
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CARD 9 CRISPR Activation Plasmid (m) | sc-436080-ACT | 20 µg | $397.00 | |||
CARD 9 CRISPR Activation Plasmid (m2) | sc-436080-ACT-2 | 20 µg | $397.00 |
Mouse Card9 encodes CARD 9, a cytosolic adaptor protein that links pattern-recognition receptors to downstream inflammatory signaling in myeloid cells. CARD 9 is a key mediator of C-type lectin receptor pathways and contributes to activation of NF-κB and MAPK programs that shape cytokine production, antimicrobial responses, and myeloid differentiation states. Through its role in innate immune signal transduction, altered CARD 9 activity is associated with dysregulated host defense and inflammation-related phenotypes in experimental models, making it relevant for studies of infection biology and immune homeostasis. Card9 is therefore frequently used to interrogate receptor-proximal signaling logic and transcriptional outputs in macrophages, dendritic cells, and neutrophil-lineage cells.
CARD 9 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Card9 expression without altering the underlying DNA sequence.
CARD 9 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Card9 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 Card9 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CARD 9 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Card9 locus and enabling the study of CARD 9-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CARD 9 pathway restoration in tumor cells with silenced or reduced Card9 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.