
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
SURF-4 CRISPR Activation Plasmid (m) | sc-423221-ACT | 20 µg | $397.00 |
Surf4 encodes SURF-4, an evolutionarily conserved endoplasmic reticulum (ER) membrane protein implicated in early secretory pathway function and ER-to-Golgi trafficking. SURF-4 participates in cargo selection and retention mechanisms that help coordinate protein sorting, secretion, and proteostasis, processes tightly linked to ER stress responses. Altered secretory trafficking and ER homeostasis are widely relevant to metabolic dysregulation, inflammation, and neurodegenerative phenotypes in model systems, making Surf4 a useful node for studying how biosynthetic load influences cell physiology. In mouse research, Surf4 modulation supports investigations of secretory pathway control across hepatocytes, immune cells, and other tissues with high secretory demand.
SURF-4 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Surf4 expression without altering the underlying DNA sequence.
SURF-4 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Surf4 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 Surf4 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SURF-4 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Surf4 locus and enabling the study of SURF-4-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SURF-4 pathway restoration in tumor cells with silenced or reduced Surf4 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.