Metaxin 2 CRISPR Activation Plasmid (h): sc-405083-ACT

MTX2 encodes metaxin 2, an outer mitochondrial membrane component of the metaxin/SAM complex that supports sorting and insertion of β-barrel proteins and contributes to mitochondrial protein import. Through its role in mitochondrial membrane biogenesis and organelle homeostasis, MTX2 influences oxidative phosphorylation capacity, mitochondrial morphology, and stress responses linked to apoptosis and proteostasis. Perturbation of mitochondrial import and membrane assembly pathways is broadly relevant to neuromuscular and neurodegenerative disease biology as well as cancer cell metabolic remodeling. MTX2 is therefore useful for interrogating mechanisms that couple mitochondrial outer membrane organization to cellular survival, energy metabolism, and organelle quality control.

Metaxin 2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MTX2 expression without altering the underlying DNA sequence.

Metaxin 2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MTX2 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 MTX2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Metaxin 2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MTX2 locus and enabling the study of Metaxin 2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Metaxin 2 pathway restoration in tumor cells with silenced or reduced MTX2 expression.

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