
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α-protein kinase 2 CRISPR Activation Plasmid (h) | sc-414073-ACT | 20 µg | $397.00 |
ALPK2 (α-protein kinase 2) is a human atypical serine/threonine kinase in the alpha-kinase family, characterized by phosphorylation of substrates within structured protein regions rather than canonical kinase motifs. It has been linked to regulation of cytoskeletal organization and cell adhesion dynamics, implicating ALPK2 in processes such as cell shape control, migration, and tissue integrity. Through these roles, ALPK2 is studied in signaling networks that coordinate mechanotransduction and cellular stress responses. Altered ALPK2 expression or function has been associated in research settings with cancer-related phenotypes and other pathologies where dysregulated proliferation, motility, or epithelial organization contributes to disease biology.
α-protein kinase 2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ALPK2 expression without altering the underlying DNA sequence.
α-protein kinase 2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ALPK2 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 ALPK2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous α-protein kinase 2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ALPK2 locus and enabling the study of α-protein kinase 2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of α-protein kinase 2 pathway restoration in tumor cells with silenced or reduced ALPK2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.