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.
ARID3B CRISPR Activation Plasmid (h): sc-411492-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- ARID3B CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- ARID3B 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 ARID3B CRISPR Activation Plasmid (h) and ARID3B CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the ARID3B 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: ARID3B Antibody (C-6): sc-514741
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ARID3B CRISPR Activation Plasmid (h) | sc-411492-ACT | 20 µg | $397.00 | |||
ARID3B CRISPR Activation Plasmid (h2) | sc-411492-ACT-2 | 20 µg | $397.00 |
ARID3B (AT-rich interaction domain 3B) encodes a DNA-binding transcription factor of the ARID family that regulates chromatin-dependent gene expression programs during development and lineage specification. By engaging AT-rich regulatory elements and cooperating with other transcriptional regulators, ARID3B influences processes such as cell fate determination, proliferation control, and differentiation-associated transcriptional networks. Altered ARID3B expression has been reported in multiple cancer contexts and other proliferative disorders, where dysregulated transcriptional control can impact pathways linked to growth, survival, and cellular identity. These features make ARID3B a useful node for studying transcriptional circuitry, epigenetic regulation, and gene regulatory network rewiring in human cells.
ARID3B CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous ARID3B expression without altering the underlying DNA sequence.
ARID3B CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the ARID3B 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 ARID3B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous ARID3B expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native ARID3B locus and enabling the study of ARID3B-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of ARID3B pathway restoration in tumor cells with silenced or reduced ARID3B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.