
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Nek11 CRISPR Activation Plasmid (h) | sc-404923-ACT | 20 µg | $397.00 |
Human NEK11 encodes the serine/threonine kinase Nek11, a NIMA-related kinase implicated in cell-cycle checkpoint control and the DNA damage response. Nek11 functions downstream of ATR/Chk1 signaling to regulate G2/M progression by modulating stability and activity of key mitotic regulators, including CDC25A, thereby coordinating replication stress responses and timely entry into mitosis. Through these roles, NEK11 contributes to maintenance of genome integrity and influences cellular sensitivity to genotoxic stress. Dysregulated checkpoint signaling and altered NEK11 activity have been linked to proliferative phenotypes and genomic instability observed across cancer-relevant contexts.
Nek11 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous NEK11 expression without altering the underlying DNA sequence.
Nek11 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the NEK11 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 NEK11 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Nek11 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native NEK11 locus and enabling the study of Nek11-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Nek11 pathway restoration in tumor cells with silenced or reduced NEK11 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.