Date published: 2026-9-4

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SELB CRISPR/Cas9 KO Plasmid (h): sc-409155

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • SELB 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 SELB 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: SELB Antibody (G-9): sc-166521
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    SELB CRISPR/Cas9 KO Plasmid (h)

    sc-409155
    20 µg
    $397.00

    Overview

    EEFSEC encodes selenocysteine-specific translation elongation factor SELB (eEFSec), a core component of the specialized machinery that inserts selenocysteine at UGA codons during synthesis of human selenoproteins. SELB cooperates with SECIS-binding factors and Sec-tRNA to support translational recoding, thereby influencing cellular redox homeostasis, oxidative stress responses, and protein quality control through selenoenzyme production. By regulating the output of antioxidant and thiol-redox pathways, EEFSEC activity can affect susceptibility to oxidative damage and stress-adaptive signaling. Dysregulation of selenoprotein biosynthesis has been associated with altered inflammatory tone and metabolic phenotypes, making EEFSEC a relevant target for mechanistic studies in disease-linked redox biology.

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

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

    Key Features

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

    Design Variants

    CRISPRs +/- HDRs

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