Date published: 2026-7-23

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LKLF/KLF2 CRISPR/Cas9 KO Plasmid (h): sc-400918

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • LKLF/KLF2 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 LKLF/KLF2 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

    LKLF/KLF2 CRISPR/Cas9 KO Plasmid (h)

    sc-400918
    20 µg
    $397.00

    Overview

    KLF2 (also known as LKLF) encodes a Krüppel-like zinc-finger transcription factor that helps maintain endothelial and immune cell homeostasis by coordinating shear stress–responsive gene programs. In vascular endothelium, KLF2 integrates mechanotransduction with transcriptional control of anti-inflammatory, anti-thrombotic, and barrier-stabilizing pathways, including modulation of nitric oxide signaling and adhesion molecule expression. In hematopoietic lineages, KLF2 influences T cell quiescence, trafficking, and differentiation through regulation of chemokine receptors and activation-associated transcriptional networks. Dysregulated KLF2 activity has been linked to vascular inflammation and atherosclerosis-related processes, and altered expression has been reported across multiple cancer and immune dysregulation contexts, supporting its use as a functional node in pathway dissection studies.

    LKLF/KLF2 CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the KLF2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the KLF2 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 KLF2 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 LKLF/KLF2 protein expression.

    This CRISPR knockout system enables efficient generation of KLF2-deficient cell models for investigation of LKLF/KLF2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting KLF2 exon(s) critical for LKLF/KLF2 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 KLF2 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by LKLF/KLF2 CRISPR/Cas9 KO Plasmid (h) and LKLF/KLF2 CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the KLF2 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by LKLF/KLF2 HDR Plasmid (h) and LKLF/KLF2 HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by KLF2 homology arms to support homology-directed repair at defined KLF2 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.