
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
VPS13D CRISPR Activation Plasmid (h) | sc-406990-ACT | 20 µg | $397.00 |
Human VPS13D encodes a large lipid transport protein that localizes at membrane contact sites and supports mitochondrial homeostasis by facilitating phospholipid transfer and organelle dynamics. VPS13D is implicated in mitochondrial fission/fusion balance, mitophagy-linked quality control, and cellular energy metabolism, connecting it to pathways governing oxidative stress responses and cytoskeletal-dependent trafficking. Disruption or dysregulation of VPS13D has been associated with neurodevelopmental and neurodegenerative phenotypes, consistent with high neuronal sensitivity to mitochondrial dysfunction. As a result, VPS13D is frequently studied in models of axonal maintenance, bioenergetic stress, and organelle crosstalk.
VPS13D CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous VPS13D expression without altering the underlying DNA sequence.
VPS13D CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the VPS13D 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 VPS13D transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous VPS13D expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native VPS13D locus and enabling the study of VPS13D-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of VPS13D pathway restoration in tumor cells with silenced or reduced VPS13D expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.