Placental lactogen II CRISPR/Cas9 KO Plasmid (m): sc-422277
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- Placental lactogen II 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 II 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
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
Placental lactogen II CRISPR/Cas9 KO Plasmid (m) | sc-422277 | 20 µg | $397.00 |
Overview
Prl3b1 encodes mouse placental lactogen II, a prolactin/growth hormone family cytokine predominantly expressed by trophoblast lineages during gestation. Placental lactogen II supports maternal–fetal adaptations by modulating endocrine and metabolic processes, including prolactin receptor (PRLR) signaling with downstream JAK2–STAT5 transcriptional programs that influence nutrient handling and maternal tissue remodeling. In the placenta, Prl3b1 activity is linked to trophoblast differentiation and regulation of maternal physiology, making it relevant for studying placental development and endocrine crosstalk. Dysregulated placental lactogen signaling has been associated with altered fetal growth and pregnancy complications in model systems, positioning Prl3b1 as a useful locus for mechanistic investigations of placental dysfunction.
Placental lactogen II CRISPR/Cas9 KO Plasmid (m) is a pool of plasmids designed for targeted disruption of the Prl3b1 gene in mouse cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the Prl3b1 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 Prl3b1 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 II protein expression.
This CRISPR knockout system enables efficient generation of Prl3b1-deficient cell models for investigation of Placental lactogen II signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
Key Features
- sgRNAs targeting Prl3b1 exon(s) critical for Placental lactogen II 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 Prl3b1 genomic sites to improve knockout efficiency
- Compatible with delivery by transfection
Design Variants
CRISPRs +/- HDRs
- gRNAs encoded by Placental lactogen II CRISPR/Cas9 KO Plasmid (m) and Placental lactogen II CRISPR/Cas9 KO Plasmid (m2) target distinct sites within the Prl3b1 locus. One or both targeting designs may be available. See Related Products for availability.
- HDR donor constructs encoded by Placental lactogen II HDR Plasmid (m) and Placental lactogen II HDR Plasmid (m2) contain a puromycin resistance cassette and an RFP reporter flanked by Prl3b1 homology arms to support homology-directed repair at defined Prl3b1 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.