
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
ALPPL2 CRISPR/Cas9 KO Plasmid (h2) | sc-401492-KO-2 | 20 µg | $397.00 |
ALPPL2 encodes alkaline phosphatase, placental-like 2, a glycosylphosphatidylinositol-anchored ectoenzyme that hydrolyzes phosphate monoesters at the cell surface. By regulating dephosphorylation of extracellular substrates, ALPPL2 can influence local phosphate availability, membrane microdomain signaling, and differentiation-associated programs, particularly in epithelial and germ cell–related contexts. Its expression is frequently used as a marker of specific developmental states, and altered ALPPL2 expression has been reported in multiple cancer-related datasets. These features make ALPPL2 relevant for studies of cell identity, surface enzyme biology, and pathway remodeling during transformation.
ALPPL2 CRISPR/Cas9 KO Plasmid (h2) is a pool of plasmids designed for targeted disruption of the ALPPL2 gene in human cell lines. Each plasmid co-expresses a unique single guide RNA (sgRNA) targeting a distinct site within the ALPPL2 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 ALPPL2 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 ALPPL2 protein expression.
This CRISPR knockout system enables efficient generation of ALPPL2-deficient cell models for investigation of ALPPL2 signaling, functional genomics studies, cancer biology research, and evaluation of therapeutic responses in human cell lines.
CRISPRs +/- HDRs
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.