Date published: 2026-7-10

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PDE3B CRISPR/Cas9 KO Plasmid (h): sc-401773

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Datasheets
  • Target species: human
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • PDE3B 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 PDE3B 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: PDE3B Antibody (F-9): sc-376823
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    Ordering Information

    Product NameCatalog #UNITPriceQtyFAVORITES

    PDE3B CRISPR/Cas9 KO Plasmid (h)

    sc-401773
    20 µg
    $397.00

    Overview

    PDE3B encodes phosphodiesterase 3B, a dual-specificity cAMP/cGMP hydrolase that shapes cyclic nucleotide microdomains and controls PKA- and PKG-dependent signaling. In adipocytes and hepatocytes, PDE3B integrates insulin and catecholamine inputs to regulate lipolysis, gluconeogenic programs, and energy storage through pathways including PI3K–AKT and downstream phosphorylation networks. In pancreatic β cells, PDE3B modulates stimulus-secretion coupling by tuning cAMP dynamics that influence insulin granule exocytosis. Dysregulated PDE3B activity has been associated with metabolic phenotypes involving insulin sensitivity, obesity-related signaling, and lipid homeostasis, supporting its utility in mechanistic studies of endocrine and cardiometabolic biology.

    PDE3B CRISPR/Cas9 KO Plasmid (h) is a pool of plasmids designed for targeted disruption of the PDE3B gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the PDE3B 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 PDE3B 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 PDE3B protein expression.

    This CRISPR knockout system enables efficient generation of PDE3B-deficient cell models for investigation of PDE3B signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting PDE3B exon(s) critical for PDE3B 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 PDE3B genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by PDE3B CRISPR/Cas9 KO Plasmid (h) and PDE3B CRISPR/Cas9 KO Plasmid (h2) target distinct sites within the PDE3B locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by PDE3B HDR Plasmid (h) and PDE3B HDR Plasmid (h2) contain a puromycin resistance cassette and an RFP reporter flanked by PDE3B homology arms to support homology-directed repair at defined PDE3B 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.