
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MLL3 CRISPR Activation Plasmid (m) | sc-437348-ACT | 20 µg | $397.00 | |||
MLL3 CRISPR Activation Plasmid (m2) | sc-437348-ACT-2 | 20 µg | $397.00 |
Kmt2c encodes the mouse histone-lysine N-methyltransferase MLL3, a SET-domain chromatin regulator that deposits H3K4 monomethylation at enhancers and helps coordinate enhancer–promoter communication. MLL3 functions in large transcriptional coactivator assemblies with roles in lineage specification, hormone receptor signaling, and developmental gene regulation. Through modulation of enhancer activity, it influences pathways controlling cell fate decisions, differentiation, and tissue homeostasis. Dysregulation of KMT2C/MLL3-associated chromatin states and transcriptional programs is implicated in disease-relevant phenotypes including altered developmental processes and oncogenic transcriptional rewiring.
MLL3 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Kmt2c expression without altering the underlying DNA sequence.
MLL3 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Kmt2c locus in human cell lines. The system is built around a catalytically inactive Cas9 (dCas9) carrying two inactivating mutations (D10A and N863A) that eliminate nuclease activity while preserving DNA binding. This dCas9 is fused to VP64, a potent transcriptional activator, and is co-expressed with a blasticidin resistance gene for selection. The second plasmid encodes the MS2-p65-HSF1 fusion protein, a secondary activator complex that works in concert with dCas9-VP64, alongside a hygromycin resistance gene. The third plasmid encodes a target-specific 20 nt sgRNA fused to two MS2 RNA aptamers that recruit the MS2-p65-HSF1 complex to the activation site, accompanied by a puromycin resistance gene. The three plasmids are delivered at a 1:1:1 mass ratio for balanced expression of all system components.
Once assembled at the target locus, the SAM complex binds within approximately 200 bp upstream of the Kmt2c transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MLL3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Kmt2c locus and enabling the study of MLL3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MLL3 pathway restoration in tumor cells with silenced or reduced Kmt2c expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.