The DPP4 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from HAP1 cells, with disruption of the DPP4 gene. This heterogeneous knockout model is suited for loss-of-function studies without clonal bias, utilizing CRISPR-mediated gene disruption to abolish DPP4 (CD26) protein expression.
HAP1 is a near-haploid human cell line from KBM-7 chronic myeloid leukemia (CML) cells. Its haploid genome facilitates efficient gene targeting, making it a powerful host for knockout studies. As a CML-derived line harboring the BCR-ABL fusion, HAP1 provides a relevant context for investigating genes involved in leukemia biology and oncogenic signaling.
DPP4 (CD26) is a transmembrane serine exopeptidase that cleaves N-terminal dipeptides from substrates including the incretins GLP-1 and GIP, thereby inactivating them and reducing insulin secretion. It also functions as a T-cell co-stimulatory molecule, interacting with ADA and caveolin-1, and cleaves chemokines like CXCL12, modulating CXCR4 signaling. Expression is regulated by TNF-??, IFN-??, IL-6, and HNF1A, linking metabolic and immune pathways. DPP4 forms complexes with tetraspanin CD9, contributing to cell adhesion and migration.
In HAP1 CML cells, DPP4 knockout enables dissection of its roles in proliferation, adhesion to fibronectin and collagen, and apoptosis. DPP4 impacts cancer progression by processing chemokines and serving as the MERS-CoV receptor; thus, this model is valuable for viral entry studies. The near-haploid background ensures clear genotype-phenotype correlations for genetic screens and drug target validation.
Applications include Western blotting for DPP4, flow cytometry for CD26, enzyme activity and GLP-1 cleavage assays, and T-cell activation studies. The model supports diabetes research (incretin regulation, DPP4 inhibitor pharmacology), immunology (TCR signaling, chemokine processing), cancer biology (migration assays, RNA-seq), and MERS-CoV entry analysis. These cells are also valuable for RNA-seq to identify DPP4-dependent transcriptional programs and for drug discovery screens targeting DPP4 or its partners. For further assistance, contact Ascent Research.
