
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
TMEM45A CRISPR Activation Plasmid (h) | sc-412437-ACT | 20 µg | $397.00 |
TMEM45A encodes a multi-pass transmembrane protein implicated in epithelial differentiation and cellular adaptation to microenvironmental stress, with reported enrichment in hypoxic and keratinizing tissues. TMEM45A has been associated with regulation of membrane trafficking and stress-response programs that influence proliferation, survival, and barrier-related processes. Transcriptional changes in TMEM45A have been observed across multiple tumor types, supporting its use as a marker-linked gene in studies of hypoxia-driven remodeling and treatment response pathways. As a membrane-localized factor with context-dependent expression, TMEM45A is frequently investigated for its contribution to tumor cell plasticity and phenotypic heterogeneity.
TMEM45A CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous TMEM45A expression without altering the underlying DNA sequence.
TMEM45A CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the TMEM45A 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 TMEM45A transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous TMEM45A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native TMEM45A locus and enabling the study of TMEM45A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of TMEM45A pathway restoration in tumor cells with silenced or reduced TMEM45A expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.