
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RBM15 CRISPR Activation Plasmid (h) | sc-417289-ACT | 20 µg | $397.00 |
RBM15 (RNA binding motif protein 15) is a nuclear RNA-binding factor that regulates gene expression through control of pre-mRNA processing and mRNA metabolism. It is implicated in hematopoietic differentiation programs and participates in transcriptional and post-transcriptional networks, including interactions with epitranscriptomic machinery that influences RNA fate decisions. Dysregulated RBM15 activity has been associated with altered lineage commitment and proliferation phenotypes, and RBM15 gene rearrangements have been reported in hematologic malignancy contexts, supporting its relevance for studying oncogenic transcriptional circuitry and RNA regulatory pathways.
RBM15 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RBM15 expression without altering the underlying DNA sequence.
RBM15 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RBM15 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 RBM15 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous RBM15 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RBM15 locus and enabling the study of RBM15-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of RBM15 pathway restoration in tumor cells with silenced or reduced RBM15 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.