Date published: 2026-8-25

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MuRF1 CRISPR/Cas9 KO Plasmid (h): sc-400797

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • MuRF1 CRISPR/Cas9 Knockout (KO) Plasmid (h) 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 MuRF1 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: MuRF1 Antibody (C-11): sc-398608
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    MuRF1 CRISPR/Cas9 KO Plasmid (h)

    sc-400797
    20 µg
    $397.00

    Overview

    TRIM63 encodes the muscle-specific E3 ubiquitin ligase MuRF1, a RING-finger protein that localizes to sarcomeric structures and promotes ubiquitin-dependent turnover of contractile and regulatory proteins. MuRF1 functions within the ubiquitin–proteasome system and coordinates with autophagy and stress-response signaling to remodel myofibrils during nutrient deprivation, denervation, and inflammatory cues. Its transcriptional and post-translational regulation intersects with FOXO-driven atrogene programs, insulin/IGF-1–AKT signaling, and NF-κB-associated catabolic pathways. Dysregulated TRIM63 activity is linked to skeletal muscle atrophy phenotypes and altered muscle homeostasis, making it a relevant node for studies of proteostasis, metabolism, and muscle wasting mechanisms.

    MuRF1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the TRIM63 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the TRIM63 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 TRIM63 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 MuRF1 protein expression.

    This CRISPR knockout system enables efficient generation of TRIM63-deficient cell models for investigation of MuRF1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting TRIM63 exon(s) critical for MuRF1 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 TRIM63 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by MuRF1 CRISPR/Cas9 KO Plasmid (h) and MuRF1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the TRIM63 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by MuRF1 HDR Plasmid (h) and MuRF1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by TRIM63 homology arms to support homology-directed repair at defined TRIM63 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.