Mnt CRISPR/Cas9 KO Plasmid (m): sc-421684
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Mnt CRISPR/Cas9 Knockout (KO) Plasmid (m) is a pool of plasmids, each encoding Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed for maximum knockout efficiency using sequences derived from the GeCKO v2 library
- gRNA sequences direct Cas9 to induce site-specific double-strand breaks (DSBs) in the Mnt genomic locus, resulting in gene knockout through non-homologous end joining (NHEJ)
- The puromycin resistance and RFP genes are flanked by LoxP sites, enabling removal of selection markers via Cre recombinase (Cre Vector: sc-418923) after establishing stable knockout cell lines
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: Mnt Antibody (F-11): sc-376708
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Mnt CRISPR/Cas9 KO Plasmid (m) | sc-421684 | 20 µg | $397.00 |
Overview
Mnt (Max network transcriptional repressor) is a basic helix–loop–helix leucine zipper factor that heterodimerizes with MAX to bind E-box elements and repress transcription, counterbalancing MYC-driven gene activation. In mouse cells, Mnt helps coordinate cell-cycle progression, differentiation, metabolism, and stress responses through regulation of MYC/MAX network targets and chromatin-associated corepressor complexes. By constraining proliferative transcriptional programs and influencing mitochondrial and ribosome biogenesis pathways, Mnt supports cellular homeostasis under mitogenic cues. Altered MNT activity or MYC–MAX–MNT network imbalance has been linked to dysregulated growth control and tumor biology, making it relevant for mechanistic studies of oncogenic transcriptional circuitry.
Mnt CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Mnt gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Mnt 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 Mnt 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 Mnt protein expression.
This CRISPR knockout system enables efficient generation of Mnt-deficient cell models for investigation of Mnt signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Mnt exon(s) critical for Mnt function
- Co-expression of SpCas9 and sgRNA from a single plasmid for simplified delivery
- GFP reporter for identification of transfected cells
- Pool of plasmids targeting multiple Mnt genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Mnt CRISPR/Cas9 KO Plasmid (m) and Mnt CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Mnt locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Mnt HDR Plasmid (m) and Mnt HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Mnt homology arms to support homology-directed repair at defined Mnt target sites corresponding to the CRISPR/Cas9 KO designs. HDR donor availability may vary. See Related Products for availability.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.