
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TMEM106B CRISPR Activation Plasmid (h) | sc-404348-ACT | 20 µg | $397.00 |
TMEM106B encodes a lysosomal transmembrane protein implicated in endolysosomal trafficking, lysosome size and acidification, and maintenance of cellular proteostasis. It interfaces with pathways controlling vesicle maturation and autophagy-lysosome function, influencing turnover of membrane proteins and aggregated cargo in the endosomal system. Genetic and expression studies have linked TMEM106B to neurodegenerative disease susceptibility and lysosomal dysfunction phenotypes, including frontotemporal dementia risk modulation. As a consequence, TMEM106B is frequently studied in neuronal and glial models to probe lysosome-centered mechanisms that shape protein clearance, stress responses, and cell survival.
TMEM106B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TMEM106B expression without altering the underlying DNA sequence.
TMEM106B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TMEM106B 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 TMEM106B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TMEM106B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TMEM106B locus and enabling the study of TMEM106B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TMEM106B pathway restoration in tumor cells with silenced or reduced TMEM106B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.