Date published: 2026-7-9

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JIP-1 CRISPR/Cas9 KO Plasmid (h): sc-401634

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • JIP-1 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 JIP-1 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: JIP-1 Antibody (2J8): sc-53552
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    JIP-1 CRISPR/Cas9 KO Plasmid (h)

    sc-401634
    20 µg
    $397.00

    Overview

    MAPK8IP1 encodes JIP-1 (JNK-interacting protein 1), a neuronal scaffold protein that organizes MAPK modules by coordinating MAP3Ks, MKK7, and JNK (MAPK8) to shape stress-activated signaling amplitude and localization. JIP-1 also interfaces with axonal transport machinery and contributes to polarized trafficking and neurite outgrowth, linking signal transduction to cytoskeletal dynamics and cargo movement. Through modulation of JNK-dependent transcriptional and apoptotic programs, MAPK8IP1 has been investigated in contexts of neurodegeneration, neuronal injury responses, and metabolic stress pathways. Dysregulated JIP-1 scaffolding can alter kinase specificity and downstream gene expression, making it a useful node for dissecting MAPK pathway wiring in human cell models.

    JIP-1 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the MAPK8IP1 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the MAPK8IP1 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 MAPK8IP1 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 JIP-1 protein expression.

    This CRISPR knockout system enables efficient generation of MAPK8IP1-deficient cell models for investigation of JIP-1 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting MAPK8IP1 exon(s) critical for JIP-1 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 MAPK8IP1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by JIP-1 CRISPR/Cas9 KO Plasmid (h) and JIP-1 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the MAPK8IP1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by JIP-1 HDR Plasmid (h) and JIP-1 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by MAPK8IP1 homology arms to support homology-directed repair at defined MAPK8IP1 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.