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.
GADD 45β CRISPR Activation Plasmid (h): sc-401286-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- GADD 45β CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- GADD 45β 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 GADD 45β CRISPR Activation Plasmid (h) and GADD 45β CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the GADD45B 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: GADD 45β Antibody (G-11): sc-377311
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
GADD 45β CRISPR Activation Plasmid (h) | sc-401286-ACT | 20 µg | $397.00 |
GADD45B (GADD45β) is a stress-inducible member of the growth arrest and DNA damage–inducible (GADD45) family that integrates genotoxic, inflammatory, and metabolic cues to modulate cell fate decisions. It participates in DNA damage response and repair-associated signaling, interfaces with MAPK pathways (including JNK and p38) and NF-κB–regulated programs, and can influence cell-cycle control, apoptosis, and cellular adaptation to stress. In human cells, dysregulated GADD45β expression has been linked to altered stress signaling and transcriptional responses observed across multiple disease contexts, including cancer biology and immune-associated pathologies. These features make GADD45β a useful molecular node for dissecting pathway crosstalk between DNA damage signaling, inflammation, and survival programs.
GADD 45β CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous GADD45B expression without altering the underlying DNA sequence.
GADD 45β CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the GADD45B 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 GADD45B transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous GADD 45β expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native GADD45B locus and enabling the study of GADD 45β-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of GADD 45β pathway restoration in tumor cells with silenced or reduced GADD45B expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.