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.
MTA2 CRISPR Activation Plasmid (h): sc-401698-ACT
- Target species: human
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- MTA2 CRISPR Activation Plasmid (h) is a synergistic activation mediator (SAM) transcription activation system designed to specifically upregulate gene expression
- MTA2 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 MTA2 CRISPR Activation Plasmid (h) and MTA2 CRISPR Activation Plasmid (h2) target distinct regulatory regions upstream of the MTA2 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: MTA2 Antibody (F-9): sc-55566
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MTA2 CRISPR Activation Plasmid (h) | sc-401698-ACT | 20 µg | $397.00 |
Human MTA2 (metastasis associated 1 family member 2) is a core component of the NuRD (nucleosome remodeling and deacetylase) complex that integrates ATP-dependent chromatin remodeling with histone deacetylation to regulate transcriptional repression programs. Through interactions with HDAC1/2, CHD3/4, and methyl-CpG binding proteins, MTA2 contributes to epigenetic control of cell cycle progression, DNA damage responses, and lineage-specific differentiation. Altered MTA2 expression and NuRD activity have been associated with oncogenic transcriptional states, epithelial–mesenchymal transition, and invasive phenotypes across multiple tumor contexts, making it a frequent focus in studies of chromatin-driven disease mechanisms. MTA2-dependent regulation of gene networks also intersects with signaling pathways that shape proliferation and stress adaptation, supporting its use as a node for dissecting transcriptional plasticity.
MTA2 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MTA2 expression without altering the underlying DNA sequence.
MTA2 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MTA2 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 MTA2 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MTA2 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MTA2 locus and enabling the study of MTA2-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MTA2 pathway restoration in tumor cells with silenced or reduced MTA2 expression.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.