MAGE-C1 Lentiviral Activation Particles (h): sc-403336-LAC

MAGEC1 encodes MAGE-C1, a cancer/testis antigen of the melanoma-associated antigen (MAGE) family with restricted expression in normal germ cells and frequent induction in malignancy. MAGE-C1 is implicated in regulation of protein homeostasis and stress-adaptive signaling through interactions that can influence ubiquitin-dependent processes and transcriptional control programs. Aberrant expression has been reported in multiple tumor contexts, including hematologic and solid cancers, where it is studied as a marker of tumor cell state and immune-relevant antigen presentation. As a human gene product, MAGE-C1 provides a useful node for dissecting epigenetic derepression, lineage-associated transcriptional programs, and proteostasis pathways linked to oncogenic phenotypes.

MAGE-C1 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 MAGEC1 upregulation across a broader range of human cell types.

MAGE-C1 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 MAGEC1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MAGE-C1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native MAGEC1 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.