
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BAT1 CRISPR Activation Plasmid (h) | sc-403785-ACT | 20 µg | $397.00 |
DDX39B encodes BAT1, an ATP-dependent RNA helicase of the DEAD-box family that participates in pre-mRNA splicing, mRNA export, and broader RNA metabolism within the nucleus. BAT1 has been linked to regulation of inflammatory signaling through modulation of cytokine gene expression and interactions with innate immune pathways, reflecting its role in coordinating transcriptional outputs with RNA processing. As a gene located in the MHC class III region, DDX39B has been studied in the context of immune-related genetic variation and susceptibility to inflammatory and autoimmune phenotypes. Dysregulation of BAT1-associated RNA processing networks can influence cell-state programs such as proliferation and stress responses, making it relevant for mechanistic studies of gene expression control.
BAT1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous DDX39B expression without altering the underlying DNA sequence.
BAT1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the DDX39B 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 DDX39B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BAT1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native DDX39B locus and enabling the study of BAT1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BAT1 pathway restoration in tumor cells with silenced or reduced DDX39B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.