CEACAM1 CRISPR Activation Plasmid (m): sc-424008-ACT

Mouse Ceacam1 encodes CEACAM1, an immunoglobulin superfamily cell adhesion receptor that mediates homophilic and heterophilic interactions at the cell surface and helps coordinate epithelial organization and intercellular communication. Through its cytoplasmic signaling motifs and isoform-specific functions, CEACAM1 modulates phosphorylation-dependent signaling networks that influence cell polarity, proliferation control, and immune cell activation states. CEACAM1 is implicated in processes such as leukocyte-endothelial interactions, mucosal barrier regulation, and tissue remodeling, linking it to inflammation-associated phenotypes and altered epithelial homeostasis. Dysregulated CEACAM1 expression has been associated with immune dysregulation and cancer-relevant changes in adhesion and signaling, supporting mechanistic studies in oncology, immunology, and host–microbe interface models.

CEACAM1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Ceacam1 expression without altering the underlying DNA sequence.

CEACAM1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Ceacam1 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 Ceacam1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CEACAM1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Ceacam1 locus and enabling the study of CEACAM1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CEACAM1 pathway restoration in tumor cells with silenced or reduced Ceacam1 expression.

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