
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HuC CRISPR Activation Plasmid (h) | sc-400172-ACT | 20 µg | $397.00 |
ELAVL3 (HuC) is a neuron-enriched RNA-binding protein that recognizes AU-rich elements in target transcripts to regulate mRNA stability, splicing, and translation, supporting neuronal differentiation and maintenance. By shaping post-transcriptional gene expression programs, HuC contributes to neurogenesis, neurite outgrowth, and synaptic function through coordinated control of RNA metabolism. Dysregulated ELAVL3 expression or localization can perturb neuronal homeostasis and has been investigated in contexts of neurodevelopmental and neurodegenerative disease biology. As a marker of post-mitotic neurons, HuC is frequently used to study lineage commitment and neuronal state changes in human cellular models.
HuC CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ELAVL3 expression without altering the underlying DNA sequence.
HuC CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ELAVL3 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 ELAVL3 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous HuC expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ELAVL3 locus and enabling the study of HuC-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of HuC pathway restoration in tumor cells with silenced or reduced ELAVL3 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.