The HDGF Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HEK293T cells with targeted disruption of the HDGF gene. This polyclonal knockout pool provides a physiologically relevant loss-of-function model for studying HDGF-dependent processes without clonal heterogeneity constraints. Ideal for investigating HDGF’s roles in proliferation, angiogenesis, and DNA repair, these cells offer a versatile tool for functional genomics studies.
The HEK293T host cell line is derived from human embryonic kidney epithelial cells and stably expresses adenovirus 5 E1A/E1B and SV40 large T antigen. Known for high transfection efficiency and robust protein expression, it is standard for viral production and CRISPR-based genome editing. Its epithelial and transformed characteristics make it suitable for dissecting growth factor and oncogenic signaling in a controlled background.
HDGF encodes a nuclear-targeted heparin-binding protein that acts as a transcriptional repressor and growth factor. It is activated by EGF, PDGF, and HGF, and regulated by FOXM1 and NF-??B. HDGF transcriptionally upregulates CCND1 (cyclin D1) and BCL2 to promote proliferation and survival, and stimulates angiogenesis via VEGFA and MMP9. It interacts with NCL, PCNA, SUMO1, and TBX2, and functions within signaling nodes involving ??-catenin, AKT1, and NFKB1, integrating growth factor signals with chromatin-associated activities to coordinate mitogenic and angiogenic responses.
In HEK293T cells, HDGF knockout impairs proliferation, DNA damage repair, and cell cycle progression, reflecting its role in mitogenic and survival signaling. The polyclonal editing captures diverse mutations, enabling assessment of functional consequences in a heterogeneous population. This model is valuable for studying HDGF’s contributions to Wnt/??-catenin, PI3K/AKT, and NF-??B pathways, and its interactions with PCNA and SUMO1 during DNA replication and repair.
These HDGF knockout polyclonal cells are suited for cancer biology, angiogenesis, and signal transduction research. Applications include proliferation (MTT/CCK-8), colony formation, flow cytometry for cell cycle and apoptosis (annexin V), migration/invasion assays, and RNA-seq. Validation by Western blot, RT-qPCR, and immunofluorescence is supported. This model aids mechanistic studies of HDGF in hepatocellular carcinoma, non-small cell lung cancer, glioma, and colorectal cancer, linking growth factor inputs to downstream targets. For further information, please contact Ascent Research.
