SLC25A11 CRISPR Activation Plasmid (h): sc-404380-ACT

SLC25A11 (mitochondrial 2-oxoglutarate/malate carrier, OGC) is an inner mitochondrial membrane solute carrier that exchanges malate for 2-oxoglutarate, linking the tricarboxylic acid (TCA) cycle with cytosolic metabolism. By supporting the malate–aspartate shuttle and mitochondrial redox balance, SLC25A11 helps regulate NADH/NAD⁺ homeostasis, anaplerosis, and oxidative metabolism. Its activity intersects with glutamine-driven carbon flux, reactive oxygen species handling, and metabolic rewiring observed in proliferative and stress-adapted cellular states. Altered SLC25A11 expression or function has been associated with metabolic dysregulation relevant to tumor biology, mitochondrial dysfunction, and susceptibility to oxidative stress in diverse experimental systems.

SLC25A11 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous SLC25A11 expression without altering the underlying DNA sequence.

SLC25A11 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the SLC25A11 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 SLC25A11 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous SLC25A11 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native SLC25A11 locus and enabling the study of SLC25A11-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of SLC25A11 pathway restoration in tumor cells with silenced or reduced SLC25A11 expression.

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