Glucose Transporter Glut3 Lentiviral Activation Particles (h): sc-400584-LAC

SLC2A3 encodes glucose transporter GLUT3 (Glut3), a high-affinity facilitative glucose transporter that supports cellular energy metabolism by mediating basal and stress-induced glucose uptake. GLUT3 contributes to glycolytic flux and links nutrient availability to downstream processes including mitochondrial respiration, redox balance, and cellular survival programs, with prominent roles in metabolically demanding contexts such as neuronal and immune cell function. Altered SLC2A3 expression has been associated with metabolic reprogramming and hypoxia-adaptive pathways, including crosstalk with HIF-1 signaling and PI3K–AKT–mTOR-regulated nutrient utilization. Dysregulated GLUT3 activity is therefore relevant to studies of inflammation, neurobiology, and cancer cell metabolism where glucose transport can shape proliferation, differentiation, and stress responses.

Glucose Transporter Glut3 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 SLC2A3 upregulation across a broader range of human cell types.

Glucose Transporter Glut3 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 SLC2A3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous Glucose Transporter Glut3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native SLC2A3 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.