
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MEK-1 CRISPR Activation Plasmid (h) | sc-400397-ACT | 20 µg | $397.00 | |||
MEK-1 CRISPR Activation Plasmid (h2) | sc-400397-ACT-2 | 20 µg | $397.00 |
MAP2K1 encodes MEK-1, a dual-specificity kinase that phosphorylates and activates ERK1/2 within the canonical RAS–RAF–MEK–ERK MAPK cascade. MEK-1 integrates signals from receptor tyrosine kinases and RAS family GTPases to regulate proliferation, differentiation, survival, and stimulus-dependent transcriptional programs. Tight control of MEK-1 activity and expression is critical for appropriate cell-cycle progression and feedback regulation across MAPK signaling networks. Dysregulation of MAP2K1/MEK-1 signaling is frequently studied in contexts of oncogenic MAPK pathway activation, developmental disorders, and mechanisms of acquired signaling rewiring.
MEK-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MAP2K1 expression without altering the underlying DNA sequence.
MEK-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MAP2K1 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 MAP2K1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MEK-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MAP2K1 locus and enabling the study of MEK-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MEK-1 pathway restoration in tumor cells with silenced or reduced MAP2K1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.