GSK3 beta Lentiviral Activation Particles (m): sc-425249-LAC

Mouse Gsk3b encodes glycogen synthase kinase 3 beta (GSK3 beta), a constitutively active serine/threonine kinase that integrates signals from PI3K–AKT, Wnt/β-catenin, and mTOR pathways to regulate phosphorylation-dependent protein turnover and transcriptional programs. GSK3 beta controls glycogen metabolism, cell-cycle progression, apoptosis, and cytoskeletal dynamics, and it modulates neuronal plasticity through effects on microtubule-associated proteins and synaptic signaling. In canonical Wnt signaling, GSK3 beta participates in the destruction complex that phosphorylates β-catenin, coupling ligand input to gene expression changes. Dysregulated Gsk3b activity is implicated in mechanisms relevant to metabolic dysfunction, inflammation, cancer-associated signaling, and neurodegeneration, making it a common target for pathway dissection in mouse models.

GSK3 beta Lentiviral Activation Particles (m) address this need by packaging the complete synergistic activation mediator (SAM) transcriptional activation system into transduction-ready, high-titer lentiviral particles, enabling efficient Gsk3b upregulation across a broader range of human cell types.

GSK3 beta Lentiviral Activation Particles (m) 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 Gsk3b transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous GSK3 beta expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Gsk3b 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.