
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
FUNDC1 CRISPR Activation Plasmid (h) | sc-403031-ACT | 20 µg | $397.00 | |||
FUNDC1 CRISPR Activation Plasmid (h2) | sc-403031-ACT-2 | 20 µg | $397.00 |
FUNDC1 (FUN14 domain containing 1) encodes an outer mitochondrial membrane receptor that regulates hypoxia- and stress-responsive mitophagy. By binding LC3 through its LIR motif and undergoing phosphorylation-dependent control, FUNDC1 helps coordinate mitochondrial quality control, organelle turnover, and bioenergetic adaptation, integrating signals from mitochondrial dynamics and oxidative stress pathways. Altered FUNDC1 activity has been linked to dysregulated mitophagy and mitochondrial dysfunction, processes relevant to neurodegeneration, ischemia-related cellular injury models, and metabolic disease mechanisms.
FUNDC1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous FUNDC1 expression without altering the underlying DNA sequence.
FUNDC1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the FUNDC1 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 FUNDC1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous FUNDC1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native FUNDC1 locus and enabling the study of FUNDC1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of FUNDC1 pathway restoration in tumor cells with silenced or reduced FUNDC1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.