
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rab 9A CRISPR Activation Plasmid (h) | sc-416915-ACT | 20 µg | $397.00 | |||
Rab 9A CRISPR Activation Plasmid (h2) | sc-416915-ACT-2 | 20 µg | $397.00 |
RAB9A encodes Rab 9A, a small GTPase that regulates late endosome dynamics and retrograde trafficking from late endosomes to the trans-Golgi network. By coordinating vesicle budding, transport, and membrane fusion, Rab 9A supports endosomal sorting, lysosomal homeostasis, and recycling of cargo such as mannose-6-phosphate receptors. This trafficking axis intersects with autophagy-lysosome pathways and broader membrane trafficking networks that shape cellular proteostasis and signaling. Dysregulated endosomal transport and Rab GTPase activity have been linked to mechanisms relevant to neurodegeneration, pathogen intracellular trafficking, and cancer cell biology, making RAB9A a useful node for mechanistic studies.
Rab 9A CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RAB9A expression without altering the underlying DNA sequence.
Rab 9A CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RAB9A 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 RAB9A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Rab 9A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RAB9A locus and enabling the study of Rab 9A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Rab 9A pathway restoration in tumor cells with silenced or reduced RAB9A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.