Arg CRISPR Activation Plasmid (h): sc-417779-ACT

ABL2 encodes Arg, a non-receptor tyrosine kinase in the Abl family that integrates signals from growth factor receptors and adhesion complexes to regulate actin cytoskeleton remodeling, cell migration, and neurite outgrowth. Arg participates in phosphorylation-dependent control of focal adhesion dynamics and Rho GTPase–linked pathways that shape cell morphology and motility. Through its roles in cytoskeletal organization and signal transduction, dysregulated ABL2 activity or expression is studied in contexts including oncogenic signaling, invasion-associated phenotypes, and aberrant kinase network activation. Human Arg is therefore a useful node for mechanistic studies of kinase-driven pathway crosstalk and cytoskeleton-dependent cellular behaviors.

Arg CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ABL2 expression without altering the underlying DNA sequence.

Arg CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ABL2 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 ABL2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Arg expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ABL2 locus and enabling the study of Arg-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Arg pathway restoration in tumor cells with silenced or reduced ABL2 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.