SDF-2 CRISPR Activation Plasmid (h): sc-404598-ACT

SDF2 encodes stromal cell–derived factor 2 (SDF-2), an endoplasmic reticulum (ER)-resident protein implicated in secretory pathway homeostasis and protein quality control. SDF-2 is associated with ER stress signaling and adaptive responses that support proper folding, maturation, and trafficking of client proteins within the early secretory system. Through its linkage to proteostasis and unfolded protein response–related processes, altered SDF2 activity is relevant to cellular phenotypes observed in conditions where ER function and secretion are disrupted, including cancer-associated stress adaptation and inflammatory microenvironments. Modulating SDF2 expression is therefore useful for dissecting how ER proteostasis interfaces with signaling outputs that influence cell survival, differentiation, and secretory capacity.

SDF-2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SDF2 expression without altering the underlying DNA sequence.

SDF-2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SDF2 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 SDF2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SDF-2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SDF2 locus and enabling the study of SDF-2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SDF-2 pathway restoration in tumor cells with silenced or reduced SDF2 expression.

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