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.
BTG2 CRISPR Activation Plasmid (h): sc-401022-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- BTG2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- BTG2 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 BTG2 CRISPR Activation Plasmid (h) and BTG2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the BTG2 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: BTG2 Antibody (1A5): sc-517187
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
BTG2 CRISPR Activation Plasmid (h) | sc-401022-ACT | 20 µg | $397.00 | |||
BTG2 CRISPR Activation Plasmid (h2) | sc-401022-ACT-2 | 20 µg | $397.00 |
BTG2 (B-cell translocation gene 2) encodes an antiproliferative, immediate-early protein that functions as a transcriptional coregulator and modulator of mRNA deadenylation, shaping gene expression programs that control cell-cycle progression and cellular stress responses. BTG2 is commonly induced downstream of p53 and integrates signaling that promotes G1/S checkpoint control, differentiation, and apoptosis through interactions with CCR4–NOT complex components and other regulatory cofactors. Altered BTG2 expression has been associated with dysregulated proliferation and genomic stability in multiple cancer-relevant contexts, and it is also linked to inflammatory and neurobiological processes via broad effects on transcriptional and post-transcriptional regulation. These properties make BTG2 a useful node for studying growth control networks, DNA damage response signaling, and context-dependent transcriptional rewiring in human cells.
BTG2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous BTG2 expression without altering the underlying DNA sequence.
BTG2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the BTG2 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 BTG2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous BTG2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native BTG2 locus and enabling the study of BTG2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of BTG2 pathway restoration in tumor cells with silenced or reduced BTG2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.