
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EpoR CRISPR Activation Plasmid (h) | sc-400442-ACT | 20 µg | $397.00 |
EPOR encodes the human erythropoietin receptor (EpoR), a type I cytokine receptor that regulates erythroid lineage survival, proliferation, and differentiation in response to erythropoietin. Ligand-dependent receptor activation promotes JAK2 phosphorylation and downstream STAT5 signaling, with additional crosstalk to PI3K–AKT and MAPK pathways that coordinate metabolic support and anti-apoptotic programs. Altered EPOR signaling has been linked to dysregulated erythropoiesis and aberrant cytokine signaling states, making it a useful node for studying hematopoietic receptor biology and signal transduction dynamics.
EpoR CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous EPOR expression without altering the underlying DNA sequence.
EpoR CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the EPOR 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 EPOR transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous EpoR expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native EPOR locus and enabling the study of EpoR-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of EpoR pathway restoration in tumor cells with silenced or reduced EPOR expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.