p38 beta MAPK11 CRISPR Activation Plasmid (h): sc-400173-ACT

MAPK11 encodes p38β, a stress-activated mitogen-activated protein kinase in the p38 MAPK family that integrates extracellular cues such as inflammatory cytokines, oxidative stress, and UV exposure into phosphorylation-dependent signaling outputs. p38β modulates transcriptional programs and post-transcriptional regulation controlling cytokine production, cell-cycle checkpoints, apoptosis, and differentiation through downstream substrates including MAPK-activated protein kinases and transcription factors. MAPK11 activity contributes to innate immune signaling and broader stress-response pathways that intersect with NF-κB-regulated inflammation and MAPK network crosstalk. Dysregulated p38 signaling has been associated with inflammatory and neurodegenerative processes and with tumor biology in a context-dependent manner, supporting mechanistic studies of pathway rewiring and stress adaptation.

p38 beta MAPK11 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MAPK11 expression without altering the underlying DNA sequence.

p38 beta MAPK11 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MAPK11 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 MAPK11 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous p38 beta MAPK11 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MAPK11 locus and enabling the study of p38 beta MAPK11-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of p38 beta MAPK11 pathway restoration in tumor cells with silenced or reduced MAPK11 expression.

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