
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α-sarcoglycan CRISPR Activation Plasmid (h) | sc-403837-ACT | 20 µg | $397.00 |
SGCA encodes human α-sarcoglycan, a core component of the sarcoglycan subcomplex within the dystrophin-associated glycoprotein complex that stabilizes the sarcolemma during muscle contraction. By linking the extracellular matrix to the actin cytoskeleton, α-sarcoglycan supports membrane integrity and mechanotransduction pathways essential for myofiber resilience. Loss or dysfunction of SGCA disrupts sarcolemmal stability, promoting contraction-induced damage and altered muscle homeostasis. SGCA is therefore widely studied in skeletal and cardiac muscle biology, membrane protein assembly, and dystrophin-complex–associated myopathies.
α-sarcoglycan CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SGCA expression without altering the underlying DNA sequence.
α-sarcoglycan CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SGCA 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 SGCA transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous α-sarcoglycan expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SGCA locus and enabling the study of α-sarcoglycan-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of α-sarcoglycan pathway restoration in tumor cells with silenced or reduced SGCA expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.