
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ULK3 CRISPR Activation Plasmid (h) | sc-403581-ACT | 20 µg | $397.00 |
ULK3 encodes a serine/threonine protein kinase in the unc-51-like kinase family that coordinates signaling events linked to cellular stress responses and morphogen-regulated transcriptional programs. ULK3 has been implicated in modulation of Hedgehog/GLI activity and cross-talk with pathways controlling autophagy, cytoskeletal dynamics, and cell-cycle progression, supporting context-dependent regulation of proliferation and differentiation. Through these network connections, ULK3 is studied in models of developmental regulation and pathway dysregulation relevant to cancer biology and fibrotic phenotypes. Altered ULK3 expression or signaling output can therefore serve as a mechanistic readout for pathway rewiring in disease-relevant cellular states.
ULK3 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ULK3 expression without altering the underlying DNA sequence.
ULK3 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ULK3 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 ULK3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ULK3 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ULK3 locus and enabling the study of ULK3-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ULK3 pathway restoration in tumor cells with silenced or reduced ULK3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.