Genome-edited Cells
Blood (peripheral blood)
The IRAK4 Knockout HL-60 Cell Line is a CRISPR/Cas9-edited human acute promyelocytic leukemia cell line with targeted disruption of the IRAK4 gene. IRAK4 encodes a serine/threonine kinase critical for MyD88-dependent signaling downstream of Toll-like receptors and interleukin-1 receptors, where it phosphorylates IRAK1 to activate NF-??B and MAPK cascades, driving pro-inflammatory cytokine production. This model is ideal for studying innate immune signaling, myeloid differentiation, IRAK4 deficiency, and screening IRAK4 inhibitors. Typical applications include western blot detection of IRAK4 and phospho-IRAK1, RT-qPCR for IL-6 and TNF-??, NF-??B reporter assays, and differentiation assays with PMA or DMSO.
DCBLD2 Knockout jurkat Polyclonal Cells
Cat. No. ARG13763
CHGA Knockout CAL27 Polyclonal Cells
Cat. No. ARG11624
ABCD4 Knockout HAP1 Polyclonal Cells
Cat. No. ARG27175
ATM Knockout HAP1 Polyclonal Cells
Cat. No. ARG34579
EGF Knockout Raji Polyclonal Cells
Cat. No. ARG40718
EPB41L1 Knockout MES-OV Polyclonal Cells
Cat. No. ARG6747
The IRAK4 Knockout HL-60 Cell Line is a CRISPR/Cas9-edited human cell line designed for loss-of-function studies of the IRAK4 gene. Based on the HL-60 acute promyelocytic leukemia line, it features targeted disruption of IRAK4, eliminating expression of the encoded serine/threonine kinase. This stable knockout model provides a uniform system for interrogating IRAK4 function in innate immune signaling without the variability of transient silencing methods.
The HL-60 cell line originates from a female patient with acute promyelocytic leukemia and serves as a classic model for myeloid differentiation. Upon treatment with DMSO or PMA, HL-60 cells differentiate into granulocyte- or monocyte/macrophage-like cells, respectively, making them valuable for studying hematopoiesis, leukemia biology, and myeloid cell function. This myeloid background is especially relevant for studying IRAK4, a key mediator of TLR and IL-1R signaling highly expressed in innate immune cells.
IRAK4 is a serine/threonine kinase essential for MyD88-dependent signaling downstream of TLRs and IL-1Rs. Ligand stimulation triggers IRAK4 recruitment to the receptor complex via MyD88, where it phosphorylates IRAK1. Activated IRAK1 engages TRAF6, leading to TAK1 and IKK activation, which promotes NF-??B nuclear translocation and MAPK (JNK, p38, ERK) signaling. This cascade induces expression of pro-inflammatory cytokines such as IL-6 and TNF-??. IRAK4 interactions with Tollip and Pellino-1/2 regulate its activity, positioning it as a non-redundant hub for innate immunity.
In the HL-60 myeloid leukemia context, IRAK4 knockout enables dissection of TLR/IL-1R pathways in a well-defined lineage model. HL-60 cells express multiple TLRs and respond to ligands like LPS and CpG DNA; IRAK4 disruption thus permits clean assessment of MyD88-dependent contributions to myeloid activation, differentiation, and leukemic cell growth. This model is particularly suited for exploring the role of innate immune signaling in AML pathogenesis and for testing IRAK4-targeted therapies in hematologic malignancies.
Applications include mechanistic studies of TLR/IL-1R signal transduction, functional complementation with wild-type or mutant IRAK4, and high-throughput screening for IRAK4 inhibitors. The line can model human IRAK4 deficiency, a primary immunodeficiency with recurrent bacterial infections. Key assays encompass western blot for IRAK4 and phospho-IRAK1, qRT-PCR for IL-6 and TNF-??, NF-??B reporter assays, cytokine ELISA, flow cytometry for TLR expression, and PMA/DMSO-driven differentiation. Additional assays such as bacterial phagocytosis and drug sensitivity can further characterize the knockout. For inquiries, please contact Ascent Research.
