Date published: 2026-7-4

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RNase T2a CRISPR/Cas9 KO Plasmid (m): sc-437175

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • RNase T2a 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 RNase T2a 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: RNase T2 Antibody (E-5): sc-393729
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    RNase T2a CRISPR/Cas9 KO Plasmid (m)

    sc-437175
    20 µg
    $397.00

    Overview

    Rnaset2a encodes the lysosomal/secreted ribonuclease RNase T2a, a member of the conserved RNase T2 family involved in RNA turnover and nucleotide recycling. RNase T2a contributes to cellular homeostasis by promoting degradation of extracellular and endolysosomal RNA, linking RNA catabolism to lysosome function and broader stress-response and inflammatory signaling pathways. In mouse models, perturbation of RNase T2 family activity is used to study how aberrant RNA persistence influences innate immune sensing, neuroinflammation, and tissue remodeling. These processes are relevant to mechanistic investigations of lysosomal storage–like phenotypes and sterile inflammation associated with dysregulated nucleic acid handling.

    RNase T2a CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Rnaset2a gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Rnaset2a 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 Rnaset2a 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 RNase T2a protein expression.

    This CRISPR knockout system enables efficient generation of Rnaset2a-deficient cell models for investigation of RNase T2a signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Rnaset2a exon(s) critical for RNase T2a 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 Rnaset2a genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by RNase T2a CRISPR/Cas9 KO Plasmid (m) and RNase T2a CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Rnaset2a locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by RNase T2a HDR Plasmid (m) and RNase T2a HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Rnaset2a homology arms to support homology-directed repair at defined Rnaset2a 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.