Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
Not CRISPR data: the image illustrates antibody quality for visualizing CRISPR experiment results.
RBMXL2 CRISPR Activation Plasmid (h): sc-409899-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- RBMXL2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- RBMXL2 CRISPR Activation Plasmid (h) consists of three plasmids at a 1:1:1 mass ratio: a plasmid encoding the deactivated Cas9 (dCas9) nuclease (D10A and N863A) fused to the transactivation domain VP64, and a blasticidin resistance gene; a plasmid encoding the MS2-p65-HSF1 fusion protein, and a hygromycin resistance gene; a plasmid encoding a target-specific 20 nt guide RNA fused to two MS2 RNA aptamers, and a puromycin resistance gene
- The resulting SAM complex binds to a site-specific region approximately 200-250 nt upstream of the transcriptional start site and provides robust recruitment of transcription factors for highly efficient gene activation
- gRNAs encoded by RBMXL2 CRISPR Activation Plasmid (h) and RBMXL2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the RBMXL2 transcriptional start site. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: RBMXL2 Antibody (RR-17): sc-101134
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
RBMXL2 CRISPR Activation Plasmid (h) | sc-409899-ACT | 20 µg | $397.00 | |||
RBMXL2 CRISPR Activation Plasmid (h2) | sc-409899-ACT-2 | 20 µg | $397.00 |
RBMXL2 encodes an RNA-binding protein with an RNA recognition motif that is implicated in pre-mRNA processing and the regulation of alternative splicing programs. As a member of the RBMX/RBMXL family, RBMXL2 is associated with post-transcriptional control of gene expression, linking splicing decisions to cell-state transitions and tissue-specific transcriptome organization. Disruption or misregulation of RNA-binding proteins and spliceosomal pathways can alter isoform balance and RNA stability, processes frequently connected to aberrant proliferation, differentiation defects, and genomic stress responses. RBMXL2 is therefore relevant for studies examining how splicing-factor networks shape RNA metabolism and influence disease-associated transcriptional phenotypes.
RBMXL2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous RBMXL2 expression without altering the underlying DNA sequence.
RBMXL2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the RBMXL2 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 RBMXL2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous RBMXL2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native RBMXL2 locus and enabling the study of RBMXL2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of RBMXL2 pathway restoration in tumor cells with silenced or reduced RBMXL2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.