The INPP5B Knockout HeLa Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the INPP5B gene has been disrupted to create a loss-of-function model. As a polyclonal pool, this product avoids the biases of single-cell cloning and provides a representative distribution of edited cells for robust functional studies of INPP5B deficiency in a widely used human cell line.
HeLa cells are an immortalized epithelial cell line derived from a human cervical adenocarcinoma. They are one of the most thoroughly characterized and commonly utilized models in biomedical research, offering reliable growth kinetics, genetic tractability, and extensive molecular annotation. Their established use in cancer biology, cell signaling, and drug discovery renders them an ideal host for investigating oncogenic pathways and phosphoinositide metabolism.
INPP5B encodes an inositol polyphosphate 5?phosphatase that selectively removes the 5?phosphate from PI(4,5)P? and PI(3,4,5)P?, two critical lipid second messengers. By depleting these phosphoinositides, INPP5B negatively regulates PI3K/AKT signaling and modulates clathrin?mediated endocytosis and actin cytoskeleton dynamics. The enzyme is activated downstream of growth factor receptors (e.g., EGFR) and functionally cooperates with OCRL, INPP5A, and PLCE1, as well as with endocytic adaptor proteins such as AP2 and clathrin. Consequently, INPP5B sits at a nexus of pathways controlling cell survival, proliferation, membrane trafficking, and cytoskeletal remodeling.
In the HeLa background, disruption of INPP5B is predicted to elevate cellular levels of PI(4,5)P? and PI(3,4,5)P?, leading to hyperphosphorylation of AKT, aberrant actin polymerization, and dysregulated endocytic trafficking. These molecular alterations can enhance migratory and invasive properties, phenocopying aspects of aggressive cancer cell behavior. This knockout population thus provides a physiologically relevant system for dissecting how phosphoinositide imbalance contributes to malignancy and for evaluating inhibitors that target the PI3K/AKT axis or endocytic pathways.
The INPP5B Knockout HeLa Polyclonal Cells are well?suited for multiple investigative areas, including the study of phosphoinositide signaling in tumor progression, the dissection of clathrin?dependent endocytosis, and the analysis of actin?based cell motility. Compatible assays range from western blotting for phospho?AKT (S473) and immunofluorescence for PIP? and F?actin to functional tests such as transferrin uptake and scratch?wound migration assays. The cells also serve as a drug?target validation platform and for screening chemical modifiers of phosphoinositide metabolism. For further details or to inquire about pricing, please contact Ascent Research.
