p38 alpha MAPK14 CRISPR Activation Plasmid (m): sc-424051-ACT
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- p38 alpha MAPK14 CRISPR Activation Plasmid (m) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- p38 alpha MAPK14 CRISPR Activation Plasmid (m) 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 p38 alpha MAPK14 CRISPR Activation Plasmid (m) and p38 alpha MAPK14 CRISPR Activation Plasmid (m2) target distinct regulatory regions upstream of the Mapk14 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: p38 alpha MAPK14 Antibody (F-9): sc-271120
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
p38 alpha MAPK14 CRISPR Activation Plasmid (m) | sc-424051-ACT | 20 µg | $397.00 | |||
p38 alpha MAPK14 CRISPR Activation Plasmid (m2) | sc-424051-ACT-2 | 20 µg | $397.00 |
Mapk14 encodes p38 alpha (MAPK14), a stress-activated serine/threonine kinase that integrates inflammatory cytokines, Toll-like receptor signals, and environmental stress into phosphorylation cascades controlling transcription, mRNA stability, and protein translation. In mouse cells, p38 alpha regulates ATF2, ELK1, and downstream kinase modules such as MAPKAPK2/3, shaping production of mediators including TNF and IL-6 and influencing cell-cycle checkpoints and apoptosis. This pathway interfaces with NF-κB and interferon signaling, linking MAPK14 activity to innate immune responses and tissue homeostasis. Dysregulated p38 signaling is widely used as a mechanistic node in models of inflammatory disease, metabolic stress, neuroinflammation, and cancer-associated microenvironmental signaling.
p38 alpha MAPK14 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Mapk14 expression without altering the underlying DNA sequence.
p38 alpha MAPK14 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Mapk14 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 Mapk14 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous p38 alpha MAPK14 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Mapk14 locus and enabling the study of p38 alpha MAPK14-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of p38 alpha MAPK14 pathway restoration in tumor cells with silenced or reduced Mapk14 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.