FOXM1 Lentiviral Activation Particles (h): sc-416676-LAC

FOXM1 (forkhead box M1) is a cell cycle–regulated transcription factor that coordinates G1/S and G2/M progression by controlling expression of genes involved in DNA replication, mitotic spindle assembly, chromatin segregation, and cytokinesis. It integrates upstream signaling from cyclin-CDK networks and checkpoint pathways, and contributes to maintenance of genomic stability through regulation of DNA damage response and repair-associated programs. Dysregulated FOXM1 expression has been linked to proliferative phenotypes, chromosomal instability, and altered differentiation states across multiple human disease contexts, including cancer biology. As a central node in proliferation and stress-response transcriptional circuits, FOXM1 is frequently studied in models of tumorigenesis, stem-like programs, and resistance to genotoxic stress.

FOXM1 Lentiviral Activation Particles (h) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient FOXM1 upregulation across a broader range of human cell types.

FOXM1 Lentiviral Activation Particles (h) deliver all functional components of the synergistic activation mediator (SAM) system via lentiviral transduction. The system comprises three particle preparations co-transduced into target cells: one encoding catalytically inactive dCas9 (D10A and N863A mutations) fused to the VP64 transactivation domain with a blasticidin resistance gene; one encoding the MS2-p65-HSF1 fusion protein with a hygromycin resistance gene; and one encoding a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers with a puromycin resistance gene. Following lentiviral transduction and genomic integration of the expression cassettes, the SAM components are stably expressed and assemble at the target locus within the proximal promoter region upstream of the FOXM1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous FOXM1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native FOXM1 genomic locus and regulatory architecture.

The lentiviral format offers several practical advantages: stable genomic integration supports heritable activation across cell divisions; high-titer particle preparations eliminate the need for in-house viral production; and compatibility with primary, non-dividing, and transfection-resistant cell types expands experimental accessibility. Successful transduction can be confirmed and enriched through triple antibiotic selection using puromycin, hygromycin, and blasticidin.

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