
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MELK Lentiviral Activation Particles (h) | sc-403062-LAC | 200 µl | $455.00 |
Maternal embryonic leucine zipper kinase (MELK) is a serine/threonine kinase implicated in regulation of cell-cycle progression, mitotic checkpoints, and progenitor-like cell states. MELK signaling interfaces with pathways governing proliferation and stress adaptation, and has been linked to control of transcriptional programs that support cell growth and survival. Dysregulated MELK expression is frequently observed in multiple tumor types and is associated with aggressive phenotypes, making it a common target for studying oncogenic signaling networks. In human cell models, MELK is used to interrogate kinase-dependent control of division, differentiation, and cellular fitness under replicative or genotoxic stress.
MELK 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 MELK upregulation across a broader range of human cell types.
MELK 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 MELK transcriptional start site, where VP64, p65, and HSF1 act cooperatively to recruit endogenous transcriptional machinery and drive sustained upregulation of endogenous MELK expression. The use of nuclease-inactive dCas9 avoids the introduction of double-strand DNA breaks and preserves the native MELK 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.