CARM1 Lentiviral Activation Particles (h): sc-404087-LAC

CARM1 (coactivator-associated arginine methyltransferase 1; PRMT4) is a protein arginine methyltransferase that catalyzes asymmetric dimethylation of histone H3 (e.g., H3R17/H3R26) and multiple non-histone substrates to regulate transcription, RNA processing, and chromatin architecture. Through coactivator functions with nuclear receptors and transcription factors, CARM1 influences programs controlling cell cycle progression, differentiation, DNA damage responses, and signal-dependent gene expression. CARM1-mediated methylation intersects with epigenetic pathways involving p300/CBP, SWI/SNF chromatin remodeling, and transcriptional elongation complexes, shaping lineage-specific and stress-responsive transcription. Dysregulated CARM1 activity and expression have been associated with oncogenic transcriptional networks and altered cellular plasticity, supporting its relevance in studies of cancer biology and hormone-responsive signaling.

CARM1 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 CARM1 upregulation across a broader range of human cell types.

CARM1 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 CARM1 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous CARM1 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native CARM1 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.