
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Sam50 CRISPR Activation Plasmid (h) | sc-404298-ACT | 20 µg | $397.00 |
SAMM50 encodes Sam50, a core component of the mitochondrial sorting and assembly machinery (SAM) complex in the outer mitochondrial membrane that mediates β-barrel protein insertion and supports mitochondrial membrane architecture. By coordinating outer membrane biogenesis and mitochondrial protein homeostasis, Sam50 influences oxidative phosphorylation capacity, mitochondrial dynamics, and stress-adaptive signaling. Perturbation of SAMM50 expression has been associated with altered mitochondrial function and has been investigated in contexts involving metabolic dysregulation and mitochondrial quality control pathways relevant to complex disease phenotypes.
Sam50 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SAMM50 expression without altering the underlying DNA sequence.
Sam50 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SAMM50 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 SAMM50 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Sam50 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SAMM50 locus and enabling the study of Sam50-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Sam50 pathway restoration in tumor cells with silenced or reduced SAMM50 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.