GLT6D1 CRISPR Activation Plasmid (h2): sc-415678-ACT-2

Human GLT6D1 (glycosyltransferase 6 domain containing 1) encodes a putative Golgi-resident glycosyltransferase implicated in the biosynthesis and remodeling of glycoconjugates, thereby influencing protein glycosylation and cell-surface carbohydrate composition. Through effects on glycan maturation, GLT6D1 is positioned to modulate secretory pathway trafficking, extracellular matrix interactions, and receptor-mediated signaling processes that depend on specific glycosylation patterns. Genetic variation and altered regulation of GLT6D1 have been linked in human studies to periodontal disease susceptibility, highlighting its relevance to host–microbe interactions and inflammatory tissue remodeling in the oral cavity. GLT6D1 gene editing and functional genomics tools support interrogation of glycosylation-dependent phenotypes, including changes in cell adhesion, immune-related signaling, and glycoproteomic profiles in disease-relevant cellular models.

GLT6D1 CRISPR Activation Plasmid (h2) provides a targeted, non-destructive approach to upregulating endogenous GLT6D1 expression without altering the underlying DNA sequence.

GLT6D1 CRISPR Activation Plasmid (h2) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GLT6D1 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 GLT6D1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GLT6D1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GLT6D1 locus and enabling the study of GLT6D1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GLT6D1 pathway restoration in tumor cells with silenced or reduced GLT6D1 expression.

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