Ggnbp2 CRISPR Activation Plasmid (m): sc-432161-ACT

Mouse Ggnbp2 (gametogenetin-binding protein 2) encodes a nuclear-associated protein implicated in germ cell biology and spermatogenesis, with reported enrichment in testis and roles linked to chromatin regulation and transcriptional control during male meiosis. Its activity is relevant to cellular programs that govern germ cell differentiation, genome integrity, and maturation of spermatids, processes that depend on coordinated DNA repair and epigenetic remodeling. Perturbation of Ggnbp2 expression has been associated with defects in male fertility phenotypes in experimental systems, supporting its use as a marker and modulator in reproductive biology studies. As a result, Ggnbp2 is of interest for investigating regulatory networks underlying germline development and testis-specific gene expression.

Ggnbp2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Ggnbp2 expression without altering the underlying DNA sequence.

Ggnbp2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Ggnbp2 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 Ggnbp2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Ggnbp2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Ggnbp2 locus and enabling the study of Ggnbp2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Ggnbp2 pathway restoration in tumor cells with silenced or reduced Ggnbp2 expression.

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