
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MLH3 Lentiviral Activation Particles (m) | sc-432245-LAC | 200 µl | $455.00 |
Mlh3 encodes MLH3, a MutL homolog that partners with MLH1 to support DNA mismatch repair and meiotic recombination, helping maintain genome stability. MLH3 contributes to repair-associated processing of recombination intermediates and has been implicated in crossover formation during meiosis, influencing chromosomal segregation and fertility-related phenotypes. Through its roles in replication error surveillance and recombination control, MLH3 intersects with pathways governing DNA damage responses and cell-cycle progression. Altered MLH3 activity or regulation is therefore relevant to studies of mutagenesis, chromosomal instability, and mismatch repair–associated disease mechanisms in mouse models.
MLH3 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 Mlh3 upregulation across a broader range of human cell types.
MLH3 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 Mlh3 transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MLH3 expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native Mlh3 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.