
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
PARD6G CRISPR Activation Plasmid (h) | sc-403179-ACT | 20 µg | $397.00 |
PARD6G encodes a human PAR-6 family scaffold protein that participates in the apical polarity complex with PAR3 and atypical PKC, coordinating establishment and maintenance of epithelial cell polarity. Through interactions that influence tight junction assembly, cytoskeletal organization, and asymmetric cell division, PARD6G contributes to regulated tissue architecture and directional cell behavior. Polarity pathway perturbations can disrupt junctional integrity and signaling networks that control proliferation and differentiation, making PARD6G relevant to studies of epithelial organization and transformation-associated phenotypes. Altered regulation of PAR complex components is also investigated in contexts such as migration and invasion biology, where polarity remodeling intersects with Rho GTPase and junctional signaling.
PARD6G CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous PARD6G expression without altering the underlying DNA sequence.
PARD6G CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the PARD6G 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 PARD6G transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous PARD6G expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native PARD6G locus and enabling the study of PARD6G-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of PARD6G pathway restoration in tumor cells with silenced or reduced PARD6G expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.