
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
α-actinin-2 CRISPR Activation Plasmid (h) | sc-401186-ACT | 20 µg | $397.00 |
ACTN2 encodes α-actinin-2, a Ca2+-sensitive actin-binding and crosslinking protein that localizes to Z-discs in striated muscle and contributes to sarcomere architecture, force transmission, and mechanosensitive remodeling. By anchoring actin filaments and coordinating multiprotein assemblies at the contractile apparatus, α-actinin-2 interfaces with cytoskeletal dynamics and signaling networks that couple adhesion, tension, and transcriptional responses. Variants or dysregulation of ACTN2 have been associated with cardiomyopathy phenotypes and arrhythmia-related risk, making it a relevant target for investigating disease-linked perturbations in myofibril organization and cardiac muscle function.
α-actinin-2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ACTN2 expression without altering the underlying DNA sequence.
α-actinin-2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ACTN2 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 ACTN2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous α-actinin-2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ACTN2 locus and enabling the study of α-actinin-2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of α-actinin-2 pathway restoration in tumor cells with silenced or reduced ACTN2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.