Genome-edited Cells
Blood (peripheral blood)
CRISPR/Cas9-mediated knockout of ELF4 in THP-1 monocytic leukemia cells. ELF4, an ETS transcription factor, is crucial for innate antiviral responses and type I interferon signaling, acting downstream of TLR4/TLR3 to regulate IFNB1 and ISGs through IRF3, NF-??B, and CBP/p300. This model facilitates studies of monocyte activation and antiviral immunity. Key applications: RT-qPCR, luciferase assays, western blot, flow cytometry, RNA-seq, and ChIP-qPCR to investigate TLR/RIG-I signaling and effector functions. Ideal for research on leukemia biology and immunodeficiency.
COPRS Knockout jurkat Polyclonal Cells
Cat. No. ARG12972
MPC2 Knockout A549 Polyclonal Cells
Cat. No. ARG10480
GNPAT Knockout Raji Polyclonal Cells
Cat. No. ARG23589
BCAR1 Knockout A549 Polyclonal Cells
Cat. No. ARG31922
PDIK1L Knockout A549 Polyclonal Cells
Cat. No. ARG10133
GCLM Knockout 786-O Polyclonal Cells
Cat. No. ARG5734
The ELF4 Knockout THP-1 Cell Line is a CRISPR/Cas9-mediated gene disruption model of the E74-like factor 4 (ELF4) locus in the human THP-1 monocytic leukemia cell line. This knockout cell line enables loss-of-function analysis of ELF4, a transcription factor essential for innate antiviral responses.
THP-1 is a well-characterized cell line derived from an acute monocytic leukemia patient, widely used to study monocyte differentiation, inflammation, and immune signaling pathways, particularly those involving Toll-like receptors (TLRs).
ELF4 is an ETS family transcription factor activated downstream of TLR4 and TLR3 through the TRIF?CTBK1?CIRF3 axis. ELF4 cooperates with IRF3, NF-??B, and the coactivator CBP/p300 to transcriptionally induce IFNB1 and interferon-stimulated genes (ISGs) such as ISG15 and OAS1. It also controls perforin and granzyme B expression. Upon TLR stimulation, ELF4 is recruited to target promoters and interacts with NF-??B and IRF3, as well as the histone acetyltransferase CBP/p300, to drive IFNB1 expression. Subsequently, type I interferon signaling through IFNAR leads to STAT1/STAT2 phosphorylation and formation of the ISGF3 complex (STAT1/STAT2/IRF9), which sustains ISG transcription, a process facilitated by ELF4. Disruption of ELF4 therefore blocks critical transcriptional programs governing type I interferon production and antiviral defense.
In the THP-1 monocytic context, ELF4 knockout impairs TLR-dependent and RIG-I-like receptor-dependent type I interferon responses, disrupting monocyte activation and antiviral restriction. This knockout cell line provides a clean genetic background to dissect ELF4-specific contributions to monocyte function, as THP-1 cells natively express TLR4, TLR3, and RIG-I. By ablating ELF4, researchers can uncouple the transcription factor from upstream signaling, revealing its role in the regulation of antiviral effectors and the establishment of an antiviral state. Moreover, because THP-1 is a leukemia-derived line, the knockout serves as a platform to study the crosstalk between innate immunity and leukemic transformation.
Typical experiments include RT-qPCR for interferon-stimulated genes (ISGs) such as ISG15 and OAS1, interferon-?? luciferase reporter assays to measure transcriptional activity at the IFNB1 promoter, and western blotting for phosphorylated STAT1 as a readout of JAK-STAT pathway activation. Flow cytometry for CD14 and CD11b monitors monocyte-to-macrophage differentiation, while RNA-seq provides a global view of transcriptional reprogramming. ChIP-qPCR assays targeting ELF4-binding motifs allow validation of direct transcriptional targets. Infection with Sendai virus or influenza A virus challenges the knockout cells, revealing defects in viral clearance and interferon production. Apoptosis assays further characterize cell death mechanisms. For further information or technical support, please contact Ascent Research.
