
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MuSK CRISPR Activation Plasmid (h) | sc-402534-ACT | 20 µg | $397.00 |
MUSK encodes muscle-specific kinase (MuSK), a receptor tyrosine kinase essential for neuromuscular junction (NMJ) development and maintenance. Upon agrin–LRP4 stimulation, MuSK signaling orchestrates acetylcholine receptor (AChR) clustering and postsynaptic differentiation through downstream pathways including Dok7- and rapsyn-associated scaffolding and cytoskeletal remodeling. This program supports synapse stabilization, muscle fiber innervation, and activity-dependent synaptic plasticity. Dysregulated MuSK signaling and NMJ instability are implicated in neuromuscular disorders, including congenital myasthenic syndromes and autoimmune myasthenia gravis subtypes.
MuSK CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MUSK expression without altering the underlying DNA sequence.
MuSK CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MUSK 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 MUSK transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MuSK expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MUSK locus and enabling the study of MuSK-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MuSK pathway restoration in tumor cells with silenced or reduced MUSK expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.