Date published: 2026-7-10

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MAF1 CRISPR/Cas9 KO Plasmid (m): sc-427213

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • MAF1 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 MAF1 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: MAF1 Antibody (H-2): sc-515614
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    MAF1 CRISPR/Cas9 KO Plasmid (m)

    sc-427213
    20 µg
    $397.00

    Overview

    Maf1 encodes MAF1, a conserved transcriptional repressor that modulates RNA polymerase III output and coordinates biosynthesis with nutrient and stress signals. In mouse cells, MAF1 activity integrates TORC1/mTOR and other kinase pathways to control tRNA and 5S rRNA transcription, linking metabolic state to proteostasis and cell growth. Through regulation of Pol III–dependent transcription, MAF1 influences proliferation, cellular stress responses, and energy homeostasis programs. Dysregulation of Pol III control and metabolic signaling pathways has been associated with altered growth phenotypes and disease-relevant processes, making Maf1 a useful node for mechanistic studies in metabolism, stress adaptation, and growth control.

    MAF1 CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Maf1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Maf1 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 Maf1 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 MAF1 protein expression.

    This CRISPR knockout system enables efficient generation of Maf1-deficient cell models for investigation of MAF1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Maf1 exon(s) critical for MAF1 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 Maf1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by MAF1 CRISPR/Cas9 KO Plasmid (m) and MAF1 CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Maf1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by MAF1 HDR Plasmid (m) and MAF1 HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Maf1 homology arms to support homology-directed repair at defined Maf1 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.