p38 gamma MAPK12 CRISPR Activation Plasmid (h): sc-400427-ACT

MAPK12 encodes p38γ, a stress-activated mitogen-activated protein kinase that integrates extracellular cues into phosphorylation-dependent programs controlling transcription, cytoskeletal dynamics, and metabolic adaptation. As part of the p38 MAPK signaling network, p38γ participates in responses to inflammatory cytokines and environmental stress, shaping downstream regulation of gene expression and protein turnover. MAPK12 activity has been implicated in cell differentiation and tissue-specific signaling, with reported links to oncogenic signaling contexts and inflammatory phenotypes where MAPK pathway rewiring is common. These attributes make p38γ MAPK12 a useful node for dissecting stress signaling crosstalk with MAPK/ERK, NF-κB–associated programs, and other kinase-driven regulatory circuits.

p38 gamma MAPK12 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MAPK12 expression without altering the underlying DNA sequence.

p38 gamma MAPK12 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MAPK12 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 MAPK12 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous p38 gamma MAPK12 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MAPK12 locus and enabling the study of p38 gamma MAPK12-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of p38 gamma MAPK12 pathway restoration in tumor cells with silenced or reduced MAPK12 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.