GLTSCR1 CRISPR Activation Plasmid (h): sc-409913-ACT

GLTSCR1 (glioma tumor suppressor candidate region gene 1) encodes a nuclear protein implicated in transcriptional regulation and chromatin-associated processes that influence cell-cycle control and differentiation programs. Reported interactions with transcriptional and epigenetic machinery suggest a role in coordinating gene expression states and maintaining nuclear organization. Altered GLTSCR1 expression or genomic disruption has been associated with cancer-related loci, including glioma-relevant regions, supporting its use as a context-dependent modulator of oncogenic transcriptional programs. As a result, GLTSCR1 is of interest for studying pathway rewiring in proliferative signaling, chromatin regulation, and stress-responsive gene expression networks.

GLTSCR1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GLTSCR1 expression without altering the underlying DNA sequence.

GLTSCR1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GLTSCR1 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 GLTSCR1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GLTSCR1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GLTSCR1 locus and enabling the study of GLTSCR1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GLTSCR1 pathway restoration in tumor cells with silenced or reduced GLTSCR1 expression.

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