NIP30 CRISPR Activation Plasmid (h): sc-404757-ACT

FAM192A encodes NIP30, a conserved human protein implicated in regulating nuclear organization and gene expression programs through protein–protein interactions at chromatin-associated complexes. Although its molecular functions are still being refined, available evidence links NIP30 to transcriptional control and RNA-associated processes that influence cell-state transitions and stress-adaptive signaling. Perturbation of these regulatory layers can affect proliferation, differentiation, and survival pathways, making NIP30 of interest for mechanistic studies in cancer biology and other disorders involving dysregulated transcriptional homeostasis. NIP30 also provides a useful node for mapping upstream regulators and downstream transcriptional networks using functional genomics approaches.

NIP30 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FAM192A expression without altering the underlying DNA sequence.

NIP30 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FAM192A 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 FAM192A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous NIP30 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FAM192A locus and enabling the study of NIP30-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of NIP30 pathway restoration in tumor cells with silenced or reduced FAM192A expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.