MTA1 CRISPR Activation Plasmid (h): sc-400942-ACT

Human MTA1 (metastasis associated 1) is a chromatin-regulatory factor best known as a core component of the NuRD (nucleosome remodeling and deacetylase) complex, linking ATP-dependent chromatin remodeling with histone deacetylation to modulate transcriptional programs. Through interactions with HDAC1/2, CHD3/4, and other NuRD subunits, MTA1 influences epigenetic control of gene expression, DNA damage responses, and cell-state transitions such as epithelial–mesenchymal plasticity. MTA1 has been studied in pathways governing proliferation, migration, and stress signaling, and altered expression is frequently associated with aggressive tumor phenotypes and metastatic behavior in multiple cancer types. Its role in reshaping enhancer and promoter accessibility makes it a useful target for dissecting transcriptional networks that couple chromatin state to oncogenic and inflammatory signaling.

MTA1 CRISPR Activation Plasmid (h) provides a targeted, non-destructive approach to upregulating endogenous MTA1 expression without altering the underlying DNA sequence.

MTA1 CRISPR Activation Plasmid (h) is a three-plasmid synergistic activation mediator (SAM) system engineered for highly efficient, site-specific transcriptional upregulation of the MTA1 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 MTA1 transcriptional start site, where VP64, p65, and HSF1 act in concert to recruit transcriptional machinery and drive upregulation of endogenous MTA1 expression. Unlike nuclease-active Cas9, dCas9 does not introduce double-strand breaks or modify the genomic sequence, preserving the native MTA1 locus and enabling the study of MTA1-dependent transcriptional responses at the endogenous locus, making it a valuable tool for functional studies, target gene identification, and the modeling of MTA1 pathway restoration in tumor cells with silenced or reduced MTA1 expression.

For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.