Date published: 2026-8-4

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Placental lactogen Iα CRISPR/Cas9 KO Plasmid (m): sc-422276

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Datasheets
  • Target species: mouse
  • 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
  • Placental lactogen Iα CRISPR/Cas9 Knockout (KO) Plasmid (m) 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 Placental lactogen Iα 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

    Placental lactogen Iα CRISPR/Cas9 KO Plasmid (m)

    sc-422276
    20 µg
    $397.00

    Overview

    Prl3d1 encodes mouse placental lactogen Iα, a prolactin/growth hormone family hormone produced predominantly by trophoblast lineages during pregnancy. Placental lactogen Iα engages prolactin receptor signaling to influence JAK2–STAT5 and related transcriptional programs that coordinate maternal metabolic adaptations and support fetal growth through endocrine and paracrine effects. In the placenta, Prl3d1 contributes to trophoblast differentiation, placental endocrine function, and regulation of nutrient allocation at the maternal–fetal interface. Dysregulation of placental lactogen pathways is commonly investigated in models of impaired placentation, fetal growth restriction, and pregnancy-associated metabolic phenotypes.

    Placental lactogen Iα CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Prl3d1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Prl3d1 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 Prl3d1 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 Placental lactogen Iα protein expression.

    This CRISPR knockout system enables efficient generation of Prl3d1-deficient cell models for investigation of Placental lactogen Iα signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.

    Key Features

    • sgRNAs targeting Prl3d1 exon(s) critical for Placental lactogen Iα 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 Prl3d1 genomic sites to improve knockout efficiency
    • Compatible with delivery by transfection

    Design Variants

    CRISPRs +/- HDRs

    • gRNAs encoded by Placental lactogen Iα CRISPR/Cas9 KO Plasmid (m) and Placental lactogen Iα CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Prl3d1 locus. One or both targeting designs may be available. See Related Products for availability.
    • HDR donor constructs encoded by Placental lactogen Iα HDR Plasmid (m) and Placental lactogen Iα HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Prl3d1 homology arms to support homology-directed repair at defined Prl3d1 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.