
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GM130 CRISPR Activation Plasmid (h) | sc-400787-ACT | 20 µg | $397.00 |
GOLGA2 encodes the cis-Golgi matrix protein GM130, a core component of the golgin network that maintains Golgi ribbon architecture and coordinates vesicle tethering and fusion. GM130 participates in ER-to-Golgi trafficking and mitotic Golgi disassembly/reassembly through interactions with proteins such as GRASP65 and the vesicle docking machinery, linking secretory pathway dynamics to cell-cycle progression. Perturbation of GM130-dependent organization can alter protein glycosylation, membrane trafficking, and organelle positioning, processes frequently implicated in cancer cell invasion, neurodegeneration, and congenital disorders affecting secretion.
GM130 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GOLGA2 expression without altering the underlying DNA sequence.
GM130 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GOLGA2 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 GOLGA2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GM130 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GOLGA2 locus and enabling the study of GM130-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GM130 pathway restoration in tumor cells with silenced or reduced GOLGA2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.