
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
HDC CRISPR Activation Plasmid (h) | sc-403606-ACT | 20 µg | $397.00 |
Human HDC encodes histidine decarboxylase, the rate-limiting enzyme that converts L-histidine to histamine, a biogenic amine that shapes inflammatory and neuroimmune signaling. Histamine produced by HDC-expressing mast cells, basophils, and other myeloid lineages modulates GPCR-driven pathways (H1–H4 receptors), influencing cytokine release, vascular permeability, and leukocyte trafficking. HDC activity also contributes to gastric acid regulation through paracrine signaling and impacts neurotransmission in the central nervous system. Dysregulated histamine biology has been linked to allergic inflammation, asthma, and other immune-mediated conditions, making HDC a useful node for studying innate immunity and tissue microenvironment signaling.
HDC CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous HDC expression without altering the underlying DNA sequence.
HDC CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the HDC 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 HDC transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous HDC expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native HDC locus and enabling the study of HDC-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of HDC pathway restoration in tumor cells with silenced or reduced HDC expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.