Date published: 2026-8-27

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ATF-5 CRISPR/Cas9 KO Plasmid (h): sc-416821

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • ATF-5 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 ATF-5 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: ATF-5 Antibody (E-10): sc-377168
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    ATF-5 CRISPR/Cas9 KO Plasmid (h)

    sc-416821
    20 µg
    $397.00

    Overview

    ATF5 encodes activating transcription factor 5 (ATF-5), a bZIP transcription factor that coordinates cellular adaptation to stress by regulating gene expression programs involved in survival, proteostasis, and differentiation. ATF-5 activity is commonly linked to integrated stress response signaling and transcriptional control downstream of eIF2α/ATF4-dependent pathways, with context-dependent roles in mitochondrial function and apoptosis. In proliferating cells, ATF-5 has been implicated in maintaining lineage state and supporting cell-cycle and metabolic remodeling under adverse conditions. Dysregulated ATF5 expression has been reported across multiple cancer models and other stress-associated pathologies, making it a useful node for mechanistic studies of stress signaling and transcriptional networks.

    ATF-5 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the ATF5 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ATF5 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 ATF5 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 ATF-5 protein expression.

    This CRISPR knockout system enables efficient generation of ATF5-deficient cell models for investigation of ATF-5 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting ATF5 exon(s) critical for ATF-5 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 ATF5 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by ATF-5 CRISPR/Cas9 KO Plasmid (h) and ATF-5 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the ATF5 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by ATF-5 HDR Plasmid (h) and ATF-5 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by ATF5 homology arms to support homology-directed repair at defined ATF5 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.