The DIP2A Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population in which the DIP2A gene has been disrupted within the HAP1 human cell line. This product provides a mixed population of edited cells, enabling loss-of-function studies without the need for single-cell clonal isolation. The knockout model is designed to facilitate investigation of DIP2A-dependent signaling and cellular phenotypes in a well-characterized host background.
HAP1 is a near-haploid human cell line originally derived from the chronic myeloid leukemia cell line KBM-7. Its haploid karyotype simplifies genetic manipulation and phenotypic analysis, making it a preferred platform for functional genomics and high-throughput genetic screens. Importantly, HAP1 cells harbor a non-functional p53 tumor suppressor, which eliminates p53-mediated responses and allows focused study of alternative signaling pathways, such as those governed by AKT.
DIP2A is a transmembrane protein that functions as a receptor for follistatin-like 1 (FSTL1), an extracellular ligand implicated in neural development and tissue homeostasis. Upon FSTL1 binding, DIP2A activates the PI3K/AKT signaling cascade, leading to phosphorylation and activation of AKT1, which in turn phosphorylates downstream targets including mTOR, GSK3B, and FOXO transcription factors. This signaling axis regulates cell survival, proliferation, and cytoskeletal dynamics. DIP2A has been implicated in axon guidance, synapse formation, and cancer progression, with particular relevance in lung adenocarcinoma and neurodevelopmental disorders such as autism spectrum disorder and intellectual disability.
In the HAP1 background, loss of DIP2A disrupts FSTL1-mediated AKT activation, offering a clean system to interrogate pathway dependencies without confounding p53 effects. The near-haploid nature of HAP1 further enhances the utility of this model, as it reduces genetic redundancy and facilitates unambiguous genotype-phenotype correlations. Researchers can use these polyclonal knockout cells to dissect the contribution of DIP2A to AKT-driven signaling networks, assess compensatory mechanisms, and identify downstream mediators critical for cell fate decisions.
This knockout model is suited for a variety of research applications, including functional genomics screens, dissection of the FSTL1-DIP2A-AKT pathway, cancer cell signaling studies, and validation of therapeutic targets. Typical assays include Western blotting for DIP2A and phospho-AKT (Ser473), RT?qPCR for DIP2A mRNA quantification, MTT?based proliferation assays, phospho-signaling analysis by immunofluorescence, and global transcriptome profiling via RNA?seq. These tools enable comprehensive characterization of DIP2A loss-of-function effects on signaling dynamics and cellular behavior. For additional technical details or ordering information, please contact Ascent Research.
