
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Rab 1A CRISPR Activation Plasmid (h) | sc-401515-ACT | 20 µg | $397.00 |
RAB1A encodes the small GTPase Rab 1A, a core regulator of ER-to-Golgi trafficking that coordinates COPII vesicle tethering, docking, and fusion to maintain secretory pathway flux and organelle homeostasis. By controlling membrane transport dynamics, Rab 1A influences Golgi organization, glycoprotein processing, autophagy-related trafficking events, and broader proteostasis networks. Perturbation of RAB1A-mediated transport has been linked to cellular stress responses and dysregulated growth signaling, making it relevant for studies of vesicular transport defects, proteostasis imbalance, and pathway rewiring in disease models. As a conserved node in intracellular logistics, Rab 1A is frequently interrogated in functional genomics workflows that connect trafficking phenotypes to signaling and metabolic outputs.
Rab 1A CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RAB1A expression without altering the underlying DNA sequence.
Rab 1A CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RAB1A 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 RAB1A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Rab 1A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RAB1A locus and enabling the study of Rab 1A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Rab 1A pathway restoration in tumor cells with silenced or reduced RAB1A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.