In Stock Cell Lines
Homo sapiens (Human)
Blood (peripheral blood)
Suspension
The DDX3Y Knockout THP-1 Cell Line is a CRISPR/Cas9-edited human monocytic leukemia cell line lacking DDX3Y, a Y-chromosome DEAD-box helicase that enhances translation of cyclin D1 and c?Myc. THP-1 cells differentiate into macrophages upon PMA treatment, enabling studies of Y-chromosome gene function, sex-specific cancer differences, and translational control. DDX3Y interacts with DDX3X, eIF4E, and stress granule components, linking growth and stress pathways. This model supports Western blotting, RT?qPCR, cell cycle analysis, stress granule assays, and translation reporter studies, aiding research in leukemia, innate immunity, and RNA biology.
CLIP1 Knockout HT29 Polyclonal Cells
Cat. No. ARG14541
ARL6IP5 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG32264
ARHGEF40 Knockout jurkat Polyclonal Cells
Cat. No. ARG33905
HS3ST1 Knockout HCT116 Polyclonal Cells
Cat. No. ARG36043
MIF Knockout CAL27 Polyclonal Cells
Cat. No. ARG11479
DENND4C Knockout 786-O Polyclonal Cells
Cat. No. ARG5222
The DDX3Y Knockout THP-1 Cell Line is a CRISPR/Cas9-edited human monocytic leukemia cell line with disruption of the DDX3Y gene, providing a stable loss-of-function model. This product enables functional studies of the Y-chromosome-encoded DEAD-box RNA helicase DDX3Y in translational control, innate immunity, and cancer, and serves as a critical tool for exploring RNA helicase biology in leukemic and immune contexts.
The parental THP-1 cell line was established from the peripheral blood of a 1-year-old male with acute monocytic leukemia. THP-1 cells grow in suspension with a diameter of ~15 ??m and can be differentiated into macrophage-like cells upon treatment with phorbol 12-myristate 13-acetate (PMA). This cell line serves as a widely used model for monocyte and macrophage function, including cytokine signaling and phagocytosis, and is a relevant background for studying leukemogenesis and innate immune pathways.
DDX3Y encodes an ATP-dependent RNA helicase that unwinds secondary structures in the 5?? UTR of target mRNAs, including cyclin D1 (CCND1) and c?Myc (MYC), thereby stimulating cap-dependent translation initiation and cell proliferation. DDX3Y activity is regulated by androgen receptor, interferon-??/??/??, and stress stimuli such as oxidative stress. It interacts with DDX3X, exportin?1 (XPO1), eIF4E, PABP1, G3BP1, and TIA1 to control the expression of interferon-stimulated genes (ISGs), the cell cycle inhibitor p21, and stress granule components, thus linking proliferative and stress-responsive pathways.
Disruption of DDX3Y in the THP-1 background is predicted to impair cap-dependent translation of CCND1 and MYC, leading to reduced proliferation and cell cycle arrest. Because DDX3Y shares functional overlap with its X-linked paralog DDX3X, this knockout line enables dissection of Y-chromosome-specific functions, sex-dependent differences in cancer, and compensatory mechanisms. Additionally, the model can be used to investigate how loss of DDX3Y affects innate immune signaling, stress granule assembly, and macrophage differentiation, providing insights into leukemia and inflammation.
Applications include Western blotting for DDX3Y, cyclin D1, and c?Myc; RT?qPCR for DDX3Y and ISGs; proliferation and cell cycle assays; RNA immunoprecipitation; stress granule immunofluorescence; cap?dependent translation reporters; apoptosis detection; RNA?seq; and cytokine ELISA. For further details, please contact Ascent Research.
