Date published: 2026-7-10

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mSHMT CRISPR/Cas9 KO Plasmid (m): sc-430789

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • mSHMT 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 mSHMT 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: mSHMT Antibody (F-11): sc-390641
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    mSHMT CRISPR/Cas9 KO Plasmid (m)

    sc-430789
    20 µg
    $397.00

    Overview

    Shmt2 encodes mitochondrial serine hydroxymethyltransferase (mSHMT), a pyridoxal phosphate–dependent enzyme that catalyzes the reversible interconversion of serine and glycine while generating 5,10-methylene-tetrahydrofolate in the mitochondrial one-carbon cycle. This activity supports folate-mediated transfer of one-carbon units required for nucleotide biosynthesis, methylation reactions, and redox homeostasis through links to NADPH production and mitochondrial metabolism. By regulating mitochondrial folate flux, SHMT2 influences proliferative programs, oxidative stress responses, and metabolic adaptation in rapidly dividing cells. Altered SHMT2 function has been associated with metabolic reprogramming and genome maintenance defects that are relevant to studies of tumor biology and mitochondrial dysfunction.

    mSHMT CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Shmt2 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Shmt2 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 Shmt2 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 mSHMT protein expression.

    This CRISPR knockout system enables efficient generation of Shmt2-deficient cell models for investigation of mSHMT signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Shmt2 exon(s) critical for mSHMT 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 Shmt2 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by mSHMT CRISPR/Cas9 KO Plasmid (m) and mSHMT CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Shmt2 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by mSHMT HDR Plasmid (m) and mSHMT HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Shmt2 homology arms to support homology-directed repair at defined Shmt2 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.