MEK-5 Lentiviral Activation Particles (h): sc-401688-LAC

MAP2K5 encodes MEK-5, a dual-specificity MAPK kinase that functions upstream of ERK5 (MAPK7) to transmit extracellular cues into transcriptional programs controlling cell proliferation, differentiation, survival, and stress responses. MEK-5 activation integrates signals from growth factors and cellular stress to regulate nuclear effectors, including MEF2 family transcription factors, thereby shaping cytoskeletal remodeling and migration-associated phenotypes. Dysregulation of the MEK5–ERK5 axis has been linked to altered growth signaling and invasive behavior across multiple disease contexts, making MAP2K5 a frequent target in pathway mapping and functional genomics studies. As a nodal kinase in MAPK cascades, MEK-5 provides a tractable handle for dissecting signaling crosstalk and downstream gene expression changes in human cells.

MEK-5 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 MAP2K5 upregulation across a broader range of human cell types.

MEK-5 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 MAP2K5 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MEK-5 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native MAP2K5 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.