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.
Estrogen Receptor beta CRISPR Activation Plasmid (r): sc-437278-ACT
- Target species: rat
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Estrogen Receptor beta CRISPR Activation Plasmid (r) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- Estrogen Receptor beta CRISPR Activation Plasmid (r) 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 Estrogen Receptor beta CRISPR Activation Plasmid (r) and Estrogen Receptor beta CRISPR Activation Plasmid (r2) target distinct regulatory regions upstream of the 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: Estrogen Receptor beta Antibody (B-1): sc-390243
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Estrogen Receptor beta CRISPR Activation Plasmid (r) | sc-437278-ACT | 20 µg | $397.00 | |||
Estrogen Receptor beta CRISPR Activation Plasmid (r2) | sc-437278-ACT-2 | 20 µg | $397.00 |
Estrogen Receptor beta (ERβ), encoded by the rat Esr2 gene, is a ligand-activated nuclear receptor that functions as a transcription factor to regulate estrogen-responsive gene networks. Upon hormone binding, ERβ modulates chromatin and recruits co-regulators to control programs involved in cell proliferation, differentiation, apoptosis, and metabolic homeostasis. ERβ signaling intersects with PI3K/AKT, MAPK/ERK, and inflammatory pathways, shaping tissue-specific responses in reproductive organs, brain, bone, and cardiovascular systems. Dysregulated ERβ activity and altered estrogen signaling balance have been implicated in hormone-responsive tumor biology, neuroinflammation, and metabolic dysfunction, making Esr2 a useful target for mechanistic studies in rat models.
Estrogen Receptor beta CRISPR Activation Plasmid (r) provides a targeted, non-destructive approach to upregulating endogenous expression without altering the underlying DNA sequence.
Estrogen Receptor beta CRISPR Activation Plasmid (r) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the 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 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous Estrogen Receptor beta expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native locus and enabling the study of Estrogen Receptor beta-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of Estrogen Receptor beta pathway restoration in tumor cells with silenced or reduced expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.