GATAD1 CRISPR Activation Plasmid (h): sc-403468-ACT

GATAD1 (GATA zinc finger domain containing 1) encodes a nuclear DNA-binding protein implicated in chromatin-associated transcriptional control through its zinc finger domain and interaction with regulatory complexes. By modulating promoter and enhancer activity, GATAD1 can influence gene expression programs linked to cell-cycle progression, cellular differentiation, and stress-responsive signaling. Altered expression or genetic perturbation of GATAD1 has been reported in multiple tumor contexts, supporting investigation into its role in oncogenic transcriptional networks and epigenetic dysregulation. This makes GATAD1 a useful target for probing how chromatin regulators shape downstream pathways that impact proliferation and genome stability.

GATAD1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GATAD1 expression without altering the underlying DNA sequence.

GATAD1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GATAD1 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 GATAD1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GATAD1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GATAD1 locus and enabling the study of GATAD1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GATAD1 pathway restoration in tumor cells with silenced or reduced GATAD1 expression.

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