
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
MTA1 CRISPR/Cas9 KO Plasmid (h) | sc-400942 | 20 µg | $397.00 |
MTA1 (metastasis associated 1) encodes a chromatin-associated coregulator and a key component of the NuRD (nucleosome remodeling and deacetylase) complex, integrating ATP-dependent nucleosome remodeling with histone deacetylation to shape transcriptional programs. Through interactions with HDAC1/2, CHD4, and sequence-specific transcription factors, MTA1 influences epithelial–mesenchymal transition, DNA damage responses, hormone receptor signaling, and cell-cycle regulation. Altered MTA1 expression or activity has been linked to tumor progression and invasive phenotypes across multiple cancer types, where it can modulate oncogenic and differentiation pathways. As a nuclear regulator of chromatin state, MTA1 is frequently studied in transcriptional repression/activation dynamics, epigenetic plasticity, and mechanisms of metastasis-associated gene expression.
MTA1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MTA1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MTA1 together with the Streptococcus pyogenes Cas9 nuclease. The plasmids also encode GFP, allowing fluorescent identification and enrichment of successfully transfected cells by fluorescence microscopy or flow cytometry.
The multi-guide design increases the likelihood of generating insertions or deletions (indels) that disrupt the MTA1 open reading frame following Cas9-mediated double-strand break formation. DNA breaks introduced by the CRISPR/Cas9 system are repaired through endogenous non-homologous end joining (NHEJ) pathways, frequently resulting in frameshift mutations that abolish MTA1 protein expression.
This CRISPR knockout system enables efficient generation of MTA1-deficient cell models for investigation of MTA1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
CRISPRs +/- HDRs
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.