
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TMEM5 CRISPR Activation Plasmid (h) | sc-411455-ACT | 20 µg | $397.00 | |||
TMEM5 CRISPR Activation Plasmid (h2) | sc-411455-ACT-2 | 20 µg | $397.00 |
TMEM5 encodes a transmembrane protein implicated in the glycosylation of α-dystroglycan, a modification required for proper extracellular matrix binding and membrane integrity. Through its role in the dystroglycan glycosylation pathway, TMEM5 contributes to cellular adhesion and tissue architecture, particularly in neuromuscular systems. Disruption of TMEM5 function has been linked to dystroglycanopathies, a class of disorders characterized by defective α-dystroglycan glycosylation and associated developmental and muscle pathology. Accordingly, TMEM5 is of interest for mechanistic studies of glycan-dependent receptor biology and membrane-associated glycosylation networks.
TMEM5 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TMEM5 expression without altering the underlying DNA sequence.
TMEM5 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TMEM5 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 TMEM5 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TMEM5 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TMEM5 locus and enabling the study of TMEM5-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TMEM5 pathway restoration in tumor cells with silenced or reduced TMEM5 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.