Genome-edited Cells
Blood (peripheral blood)
The CXCR2 Knockout THP-1 Cell Line is a CRISPR/Cas9-edited human knockout cell line with disruption of the CXCR2 chemokine receptor gene in the THP-1 monocytic leukemia host. CXCR2, activated by chemokines including CXCL1 and IL-8 (CXCL8), couples to G??i and triggers PI3K/AKT and ERK1/2 cascades, promoting leukocyte migration and expression of factors such as MMP-9 and VEGF. This model supports research into inflammatory signaling, cancer metastasis, and immune cell trafficking, and is suited for Transwell migration, calcium mobilization, and phospho-ERK analyses. The THP-1 background offers a human monocyte/macrophage system for chemokine pathway interrogation and drug target studies.
ADAM9 Knockout HEK293T Polyclonal Cells
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HLTF Knockout 786-O Polyclonal Cells
Cat. No. ARG25263
ARSB Knockout huh-7 Polyclonal Cells
Cat. No. ARG27998
IQGAP1 Knockout HAP1 Polyclonal Cells
Cat. No. ARG36984
DSTYK Knockout HAP1 Polyclonal Cells
Cat. No. ARG39862
Human Skeletal Muscle Cells
Cat. No. ARP0160
The CXCR2 Knockout THP-1 Cell Line is a CRISPR/Cas9-edited human knockout cell line derived from the THP-1 monocytic leukemia cell line, providing a genetically defined loss-of-function model for chemokine receptor-mediated signaling studies. This stable knockout enables long-term functional analysis without pharmacological off-target effects and is supplied as a ready-to-use continuous culture. The cell line eliminates CXCR2 protein expression, allowing precise attribution of biological responses to this receptor.
The THP-1 cell line originates from the peripheral blood of a patient with acute monocytic leukemia and is a benchmark model for human monocyte and macrophage function. These cells can be differentiated into adherent, macrophage-like cells by treatment with phorbol esters or cytokines, enabling detailed studies of inflammatory responses, phagocytosis, and chemotaxis. Their robust chemokine responsiveness and well-characterized signaling make them an ideal platform for deconstructing receptor-specific contributions through gene knockout.
CXCR2 is a G protein-coupled receptor activated by ELR+ CXC chemokines, notably CXCL1, CXCL2, CXCL5, and IL-8 (CXCL8). Upon binding, it couples to G??i proteins, stimulating PLC??-mediated calcium mobilization and initiating PI3K/AKT and MAPK/ERK1/2 signaling. Receptor regulation involves phosphorylation by GRK2 and GRK5, followed by ??-arrestin recruitment and internalization. Downstream, these pathways activate NF-??B and drive expression of MMP-9, VEGF, and other pro-inflammatory mediators, thus coordinating leukocyte migration, survival, and angiogenic programs.
Loss of CXCR2 in THP-1 cells abrogates chemokine-induced calcium flux, ERK1/2 phosphorylation, and directional migration, establishing a clean system for dissecting inflammatory signaling and immune cell trafficking. This knockout line is particularly relevant to chronic inflammatory diseases such as rheumatoid arthritis, COPD, and psoriasis, as well as to cancer metastasis research, where CXCR2 facilitates tumor cell invasion and angiogenesis. Differentiation of the knockout cells into macrophage-like phenotypes further allows investigation of receptor-dependent functions in phagocytosis, cytokine release, and tissue infiltration.
The CXCR2 Knockout THP-1 Cell Line supports a range of assays, including Transwell migration to quantify chemotaxis, calcium mobilization to monitor G protein activation, and phospho-ERK analysis by Western blotting. Transcriptional outcomes can be measured by RT-qPCR for targets like MMP-9 and VEGF, while secretory profiles are assessed via ELISA. Applications encompass cancer metastasis studies, inflammatory disease modeling, chemokine pathway dissection, and drug target validation. For technical inquiries, contact Ascent Research.
