Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
MEK kinase-3 CRISPR Activation Plasmid (h): sc-404290-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MEK kinase-3 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- MEK kinase-3 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting 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 MEK kinase-3 CRISPR Activation Plasmid (h) and MEK kinase-3 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the MAP3K3 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: MEK kinase-3 Antibody (40): sc-136260
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MEK kinase-3 CRISPR Activation Plasmid (h) | sc-404290-ACT | 20 µg | $397.00 |
Human MAP3K3 encodes MEK kinase-3 (MAP3K3), a serine/threonine MAP kinase kinase kinase that integrates upstream cues from cytokine receptors, Toll-like receptors, and cellular stress to propagate signaling through MAPK cascades. MAP3K3 contributes to regulation of NF-κB and MAPK-driven transcriptional programs affecting inflammation, cell survival, differentiation, and cytoskeletal dynamics. Through these networks, MAP3K3 influences endothelial and immune cell responses, including pathways linked to angiogenic signaling and innate immune activation. Dysregulated MAP3K3 activity and altered pathway wiring have been associated with inflammatory states and oncogenic signaling contexts, supporting its utility as a node for mechanistic pathway studies.
MEK kinase-3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MAP3K3 expression without altering the underlying DNA sequence.
MEK kinase-3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MAP3K3 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 MAP3K3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MEK kinase-3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MAP3K3 locus and enabling the study of MEK kinase-3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MEK kinase-3 pathway restoration in tumor cells with silenced or reduced MAP3K3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.