AGGF1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the Jurkat T lymphoblast cell line, with targeted disruption of the angiogenic factor AGGF1. This loss-of-function model is generated via CRISPR/Cas9-mediated gene editing to create a heterogeneous pool of cells carrying diverse genetic alterations at the AGGF1 locus. As a polyclonal population, it minimizes clonal selection artifacts and provides a faithful representation of gene knockout effects for downstream functional studies.
The Jurkat host is an immortalized human T-cell line established from the peripheral blood of a 14-year-old male with acute T-cell leukemia. It is extensively used as a model system for T-cell receptor signaling, activation, apoptosis, and cancer biology. Jurkat cells proliferate rapidly in suspension, exhibit well-characterized signaling networks, and are highly amenable to genetic manipulation, making them a versatile platform for studying gene function in a leukemic T-cell context.
AGGF1 is a secreted angiogenic protein that promotes endothelial cell proliferation, migration, and tube formation by activating the PI3K/AKT and ERK1/2 signaling pathways. It functions downstream of hypoxia (HIF1A) and pro-inflammatory cytokines, and its activity is mediated through interactions with cell surface receptors such as VEGFR2, integrins, and fibronectin. Upon binding, AGGF1 triggers phosphorylation cascades involving PI3K, AKT, and ERK1/2, driving cellular processes critical for vascular development. Genetic mutations in AGGF1 are associated with Klippel-Trenaunay syndrome and aberrant tumor angiogenesis.
Although AGGF1 is canonically an endothelial factor, its knockout in Jurkat T cells allows investigation of its potential roles in immune cell signaling and leukemia biology. The Jurkat line??s robust PI3K/AKT and MAPK/ERK pathways provide a clean background to dissect AGGF1-dependent signaling independent of endothelial-specific effects. This model is useful for examining whether AGGF1 contributes to T-cell proliferation, survival, or apoptosis, and for exploring how angiogenic pathways may cross-talk with oncogenic signaling in hematopoietic malignancies.
Applications include genomic PCR and sequencing to validate gene disruption, RT-qPCR and western blotting to confirm loss of AGGF1 expression, and phospho-AKT/ERK analysis to assess signaling changes. Functional assays such as flow cytometry for apoptosis and cell proliferation assays can delineate phenotypic consequences. These knockout cells serve as a tool for studying angiogenic signaling, screening AGGF1-targeted therapies, and modeling vascular malformation disorders. For further information or custom gene editing services, contact Ascent Research.
