
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MAPKAP-1 CRISPR Activation Plasmid (h) | sc-404288-ACT | 20 µg | $397.00 |
MAPKAP1 encodes MAPKAP-1 (also known as mSIN1), an essential component of mechanistic target of rapamycin complex 2 (mTORC2) that helps determine complex assembly, substrate selectivity, and subcellular localization. Through mTORC2, MAPKAP-1 supports phosphorylation of AGC-family kinases such as AKT (Ser473), SGK, and PKC, linking growth factor signaling to cell survival, metabolism, cytoskeletal remodeling, and migration. MAPKAP1-dependent signaling intersects with PI3K–AKT–mTOR networks that are frequently perturbed in cancer biology and metabolic dysregulation. Altered MAPKAP1 expression or pathway activity has been associated with changes in proliferative capacity, stress responses, and invasive phenotypes in diverse cellular contexts.
MAPKAP-1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MAPKAP1 expression without altering the underlying DNA sequence.
MAPKAP-1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MAPKAP1 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 MAPKAP1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MAPKAP-1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MAPKAP1 locus and enabling the study of MAPKAP-1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MAPKAP-1 pathway restoration in tumor cells with silenced or reduced MAPKAP1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.