Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
CCDC109A CRISPR Activation Plasmid (h): sc-413850-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- CCDC109A CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- CCDC109A CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by CCDC109A CRISPR Activation Plasmid (h) and CCDC109A CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the MCU transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: CCDC109A Antibody (E-9): sc-515930
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
CCDC109A CRISPR Activation Plasmid (h) | sc-413850-ACT | 20 µg | $397.00 |
MCU (CCDC109A) encodes the pore-forming subunit of the mitochondrial calcium uniporter complex, enabling Ca2+ uptake across the inner mitochondrial membrane to couple cytosolic Ca2+ signals to mitochondrial metabolism. By shaping matrix Ca2+ levels, MCU influences activation of TCA cycle dehydrogenases, oxidative phosphorylation efficiency, reactive oxygen species signaling, and susceptibility to permeability transition during stress. This mitochondrial Ca2+ axis intersects with apoptosis regulation, bioenergetic adaptation, and Ca2+-dependent transcriptional programs that govern proliferation and differentiation. Dysregulated MCU activity has been implicated in contexts of altered metabolic state and mitochondrial stress responses, including studies of cancer cell remodeling, ischemic injury mechanisms, and neuromuscular and neurodegenerative phenotypes where Ca2+ handling is disrupted.
CCDC109A CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MCU expression without altering the underlying DNA sequence.
CCDC109A CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MCU 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 MCU transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous CCDC109A expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MCU locus and enabling the study of CCDC109A-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of CCDC109A pathway restoration in tumor cells with silenced or reduced MCU expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.