FOXM1 CRISPR Activation Plasmid (h): sc-416676-ACT

FOXM1 (forkhead box M1) is a proliferation-associated transcription factor that coordinates cell-cycle progression by regulating genes required for the G1/S transition and mitotic entry, including pathways controlling DNA replication, spindle assembly, and chromosome segregation. It interfaces with key regulatory networks such as CDK–cyclin signaling and DNA damage response programs to balance cell division with genome integrity. Aberrant FOXM1 expression is frequently observed in oncology-related transcriptional signatures and is linked to invasive growth, genomic instability, and altered cellular stress responses, making it a widely used node for studying tumor biology and cell-cycle control. In addition, FOXM1 contributes to tissue remodeling programs by influencing epithelial–mesenchymal traits and transcriptional responses to oxidative and replicative stress.

FOXM1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FOXM1 expression without altering the underlying DNA sequence.

FOXM1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FOXM1 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 FOXM1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FOXM1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FOXM1 locus and enabling the study of FOXM1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FOXM1 pathway restoration in tumor cells with silenced or reduced FOXM1 expression.

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