Date published: 2026-7-3

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FAM83B CRISPR/Cas9 KO Plasmid (h): sc-415158

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • FAM83B 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 FAM83B 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
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    FAM83B CRISPR/Cas9 KO Plasmid (h)

    sc-415158
    20 µg
    $397.00

    Overview

    FAM83B (family with sequence similarity 83 member B) is a cytoplasmic signaling adaptor implicated in amplification of receptor tyrosine kinase outputs and downstream MAPK/ERK pathway activity, supporting proliferative and survival programs in epithelial cells. It has been linked to modulation of EGFR/RAS signaling dynamics and crosstalk with PI3K-associated processes, influencing transcriptional responses and cell-cycle progression. Dysregulated FAM83B expression has been reported in multiple tumor contexts and is studied as a contributor to oncogenic signaling robustness, therapy tolerance phenotypes, and altered growth-factor dependence. These features make FAM83B a useful node for dissecting pathway wiring, feedback control, and genotype–phenotype relationships in cancer biology models.

    FAM83B CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the FAM83B gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the FAM83B 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 FAM83B 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 FAM83B protein expression.

    This CRISPR knockout system enables efficient generation of FAM83B-deficient cell models for investigation of FAM83B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting FAM83B exon(s) critical for FAM83B 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 FAM83B genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by FAM83B CRISPR/Cas9 KO Plasmid (h) and FAM83B CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the FAM83B locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by FAM83B HDR Plasmid (h) and FAM83B HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by FAM83B homology arms to support homology-directed repair at defined FAM83B 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.