
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
EAF1 CRISPR Activation Plasmid (m) | sc-428881-ACT | 20 µg | $397.00 |
Mouse Eaf1 encodes EAF1, a nuclear transcriptional cofactor originally characterized as an ELL-associated factor that helps coordinate RNA polymerase II elongation and gene expression programs. EAF1 participates in chromatin-associated regulatory complexes and has been linked to control of cell cycle progression, differentiation, and stress-responsive transcriptional outputs. Through its role in transcriptional regulation, EAF1 can influence pathways governing proliferation and developmental gene networks, making it relevant to studies of dysregulated transcription in cancer biology and other contexts where gene expression control is perturbed. Investigating Eaf1 function supports mechanistic dissection of transcriptional elongation and promoter-proximal regulatory events in mammalian cells.
EAF1 CRISPR Activation Plasmid (m) provides a targeted, non-destructive approach to upregulating endogenous Eaf1 expression without altering the underlying DNA sequence.
EAF1 CRISPR Activation Plasmid (m) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the Eaf1 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 Eaf1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous EAF1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native Eaf1 locus and enabling the study of EAF1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of EAF1 pathway restoration in tumor cells with silenced or reduced Eaf1 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.