CD71/TFRC/Transferrin Receptor Lentiviral Activation Particles (h): sc-400310-LAC

TFRC (CD71) encodes the transferrin receptor, a type II membrane glycoprotein that mediates clathrin-dependent endocytosis of transferrin-bound iron and supports intracellular iron homeostasis. By regulating iron uptake and availability, CD71 influences heme synthesis, mitochondrial respiration, DNA replication, and redox balance, linking nutrient sensing to proliferative metabolism. TFRC expression is tightly coordinated with cell cycle programs and is often elevated in rapidly dividing cells, where altered iron handling can reshape oxidative stress responses and metabolic rewiring. Dysregulated TFRC activity and trafficking have been associated with oncogenic growth, anemia-related phenotypes, and perturbations of immune cell activation and differentiation.

CD71/TFRC/Transferrin Receptor 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 TFRC upregulation across a broader range of human cell types.

CD71/TFRC/Transferrin Receptor 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 TFRC transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CD71/TFRC/Transferrin Receptor expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native TFRC 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.