
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rab 7 CRISPR Activation Plasmid (h) | sc-400465-ACT | 20 µg | $397.00 |
RAB7A encodes Rab 7, a small GTPase that regulates late endosome maturation, endosome–lysosome trafficking, and lysosomal biogenesis. By coordinating vesicle motility, tethering, and fusion events, Rab 7 supports cargo degradation, receptor downregulation, and autophagosome–lysosome fusion within the endolysosomal system. This pathway intersects with nutrient sensing and cellular stress responses, influencing mitochondrial quality control and proteostasis. Dysregulated RAB7A activity has been linked to neurodegenerative and neuropathic phenotypes, altered pathogen entry/replication, and cancer-associated changes in trafficking and signaling outputs.
Rab 7 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RAB7A expression without altering the underlying DNA sequence.
Rab 7 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RAB7A 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 RAB7A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Rab 7 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RAB7A locus and enabling the study of Rab 7-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Rab 7 pathway restoration in tumor cells with silenced or reduced RAB7A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.