TMEM106C CRISPR Activation Plasmid (h): sc-413113-ACT

TMEM106C encodes a predicted multi-pass transmembrane protein that is thought to contribute to membrane organization and protein trafficking within the secretory and endolysosomal system. As a member of the TMEM106 family, TMEM106C is studied in the context of organelle homeostasis, vesicular transport, and regulation of protein turnover, processes that intersect with cellular stress responses and signaling networks. Altered expression of transmembrane trafficking regulators can reshape lysosomal function, autophagy flux, and downstream inflammatory or metabolic signaling. These mechanisms make TMEM106C a useful target for investigating how membrane compartment dynamics influence cell-state transitions and disease-associated phenotypes in human model systems.

TMEM106C CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TMEM106C expression without altering the underlying DNA sequence.

TMEM106C CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TMEM106C 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 TMEM106C transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TMEM106C expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TMEM106C locus and enabling the study of TMEM106C-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TMEM106C pathway restoration in tumor cells with silenced or reduced TMEM106C expression.

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