Dyrk1B CRISPR Activation Plasmid (h): sc-403880-ACT

DYRK1B encodes dual-specificity tyrosine phosphorylation–regulated kinase 1B (Dyrk1B), a serine/threonine kinase that modulates cell-cycle progression, cellular quiescence, and differentiation programs through phosphorylation of regulatory proteins. Dyrk1B activity intersects with signaling networks controlling stress responses and metabolic homeostasis, including pathways influencing transcriptional control, protein turnover, and growth-factor–dependent signaling. Altered DYRK1B expression or kinase activity has been associated with dysregulated proliferation and survival phenotypes, making it relevant to studies of oncogenic signaling, tissue remodeling, and metabolic disease biology. As an endogenous regulator of kinase-driven signaling outputs, DYRK1B is frequently investigated for its role in pathway crosstalk and context-dependent control of gene expression states.

Dyrk1B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DYRK1B expression without altering the underlying DNA sequence.

Dyrk1B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DYRK1B 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 DYRK1B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Dyrk1B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DYRK1B locus and enabling the study of Dyrk1B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Dyrk1B pathway restoration in tumor cells with silenced or reduced DYRK1B expression.

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