
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GLULD1 CRISPR Activation Plasmid (h) | sc-409944-ACT | 20 µg | $397.00 |
Human LGSN encodes GLULD1 (also known as lengsin), a lens-enriched protein implicated in maintaining crystallin protein homeostasis and cellular architecture during lens fiber cell differentiation. Functional studies link LGSN/GLULD1 to cytoskeletal organization and proteostasis processes that support transparency and resistance to aggregation in ocular tissues. Altered expression or dysfunction of lens structural maintenance factors is relevant to cataract biology and other disorders characterized by protein misfolding and compromised lens integrity. These features make LGSN a useful target for investigating tissue-specific differentiation programs and stress responses that impact proteome stability.
GLULD1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous LGSN expression without altering the underlying DNA sequence.
GLULD1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the LGSN 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 LGSN transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GLULD1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native LGSN locus and enabling the study of GLULD1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GLULD1 pathway restoration in tumor cells with silenced or reduced LGSN expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.