
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
LRP CRISPR Activation Plasmid (m) | sc-429657-ACT | 20 µg | $397.00 | |||
LRP CRISPR Activation Plasmid (m2) | sc-429657-ACT-2 | 20 µg | $397.00 |
Mouse Mvp encodes LRP (major vault protein), the principal structural component of vault ribonucleoprotein particles implicated in cytoplasmic trafficking, nucleocytoplasmic transport, and stress-responsive signaling. LRP interacts with pathways regulating xenobiotic handling and cellular homeostasis, including drug transport and detoxification processes, and has been linked to modulation of PI3K/AKT and MAPK-associated responses in some contexts. Altered MVP/LRP expression has been associated with multidrug resistance phenotypes and changes in apoptotic sensitivity, making it relevant to studies of tumor cell adaptation and treatment response. In immune and epithelial systems, vault particle biology is also connected to innate defense programs and inflammation-related signaling, supporting investigation across cancer and host-response models.
LRP CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Mvp expression without altering the underlying DNA sequence.
LRP CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Mvp 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 Mvp transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous LRP expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Mvp locus and enabling the study of LRP-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of LRP pathway restoration in tumor cells with silenced or reduced Mvp expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.