MLL3 Lentiviral Activation Particles (m): sc-437348-LAC
- Target species: mouse
- 200 µl of transduction-ready, high-titer CRISPR/dCas9 Lentiviral Activation Particles
- MLL3 Lentiviral Activation Particles (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically and efficiently upregulate gene expression via lentiviral transduction of cells
- MLL3 Lentiviral Activation Particles (m) contain the following SAM Activation elements: a deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, an MS2-p65-HSF1 fusion protein and a target-specific 20 nt guide RNA. They also contain the blasticidin, hygromycin and puromycin resistance genes
- Upon transduction, the SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by MLL3 Lentiviral Activation Plasmid (m) and MLL3 Lentiviral Activation Plasmid (m2) target distinct regulatory regions of the Kmt2c promoter. One or both designs may be available
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MLL3 Lentiviral Activation Particles (m) | sc-437348-LAC | 200 µl | $455.00 |
Kmt2c encodes the mouse histone lysine methyltransferase MLL3, a COMPASS-like chromatin regulator that catalyzes H3K4 mono- and di-methylation at enhancers to shape transcriptional programs. MLL3 cooperates with nuclear receptor and lineage-determining transcription factors to control enhancer priming, RNA polymerase II dynamics, and cell identity decisions during development and differentiation. Through its effects on chromatin accessibility and long-range regulatory elements, MLL3 influences pathways linked to metabolism, inflammation, and DNA damage responses. Dysregulation of Kmt2c/MLL3-dependent enhancer function is associated with altered gene expression networks observed across multiple disease-relevant contexts, including cancer-associated epigenetic remodeling.
MLL3 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 Kmt2c upregulation across a broader range of human cell types.
MLL3 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 Kmt2c transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MLL3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Kmt2c 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.