
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MAGE-L2 CRISPR Activation Plasmid (m) | sc-424255-ACT | 20 µg | $397.00 |
Mouse Magel2 encodes MAGE-L2, a member of the melanoma antigen (MAGE) family implicated in hypothalamic neuroendocrine regulation and neuronal development. MAGE-L2 participates in ubiquitin-dependent protein homeostasis through interactions with E3 ubiquitin ligase complexes, influencing trafficking and turnover of key cellular proteins. Magel2 activity has been linked to regulation of circadian rhythm, energy balance, and leptin-melanocortin signaling pathways that shape feeding behavior and metabolism. Dysregulation of MAGEL2 is associated with neurodevelopmental and metabolic phenotypes, making it a useful target for mechanistic studies of hypothalamic circuitry and proteostasis.
MAGE-L2 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Magel2 expression without altering the underlying DNA sequence.
MAGE-L2 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Magel2 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 Magel2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MAGE-L2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Magel2 locus and enabling the study of MAGE-L2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MAGE-L2 pathway restoration in tumor cells with silenced or reduced Magel2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.