Date published: 2026-7-16

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UROD CRISPR/Cas9 KO Plasmid (m): sc-423626

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • UROD 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 UROD 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: UROD Antibody (C-4): sc-365297
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    UROD CRISPR/Cas9 KO Plasmid (m)

    sc-423626
    20 µg
    $397.00

    Overview

    Mouse Urod encodes uroporphyrinogen decarboxylase (UROD), a cytosolic enzyme in the heme biosynthesis pathway that catalyzes decarboxylation of uroporphyrinogen III to coproporphyrinogen III. This step supports cellular tetrapyrrole flux and proper production of heme required for mitochondrial respiration, cytochrome function, and redox homeostasis. Disruption of UROD activity alters porphyrin metabolism, promoting accumulation of porphyrin intermediates and associated oxidative stress responses. UROD-dependent defects are relevant to porphyrias and provide a mechanistic entry point to study metabolic stress, iron/heme regulation, and hepatocyte or erythroid lineage biology.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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