SSc5D CRISPR Activation Plasmid (h): sc-418823-ACT

SSC5D encodes the human scavenger receptor cysteine-rich family member with multiple SRCR domains (SSc5D), a pattern-recognition and cell-interaction protein implicated in innate immune surveillance. SSc5D has been associated with modulation of inflammatory signaling and regulation of leukocyte activation states, linking it to pathways governing host–microbe interactions and tissue immune homeostasis. Expression patterns in myeloid-lineage and immune-associated contexts make SSC5D relevant for studying mechanisms that shape antigen-presenting cell function, cytokine responses, and immune cell trafficking. Dysregulated SSC5D expression has been reported in inflammatory and immune-related disease settings, supporting its use as a molecular entry point for investigating disease-associated immune phenotypes.

SSc5D CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SSC5D expression without altering the underlying DNA sequence.

SSc5D CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SSC5D 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 SSC5D transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SSc5D expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SSC5D locus and enabling the study of SSc5D-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SSc5D pathway restoration in tumor cells with silenced or reduced SSC5D expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.