In Stock Cell Lines
Homo sapiens (Human)
Blood (peripheral blood)
Suspension
The C5 Knockout THP-1 Cell Line is a CRISPR/Cas9-edited cell line lacking complement component C5, disrupting C5a-mediated inflammation and C5b-dependent MAC formation. Utilizing the THP-1 monocytic leukemia model, this knockout line allows investigation of terminal complement pathway functions in macrophage-driven innate immunity. Ideal for drug screening, complement disease modeling, and inflammatory signaling studies, this cell line supports assays such as C5a ELISA, chemotaxis analysis, and cytokine profiling. Key molecular interactors include C5aR1, C6?CC9, and NLRP3, positioned downstream of complement activation.
ARHGEF28 Knockout huh-7 Polyclonal Cells
Cat. No. ARG27975
KHDRBS1 Knockout A2780 Polyclonal Cells
Cat. No. ARG29299
CCL8 Knockout HAP1 Polyclonal Cells
Cat. No. ARG43205
CASP1 Knockout huh-7 Polyclonal Cells
Cat. No. ARG28190
PCYOX1L Knockout MES-OV Polyclonal Cells
Cat. No. ARG6234
MAT2B Knockout Raji Polyclonal Cells
Cat. No. ARG2015
The C5 Knockout THP-1 Cell Line is a CRISPR/Cas9-mediated C5 knockout derivative of the THP-1 human monocytic leukemia cell line. This cell line provides a stable genetic disruption of the complement component C5 gene, eliminating its expression and allowing researchers to investigate C5-dependent pathways in innate immunity and inflammation. The product is supplied as a validated, antibiotic-free cell culture ready for downstream in vitro applications.
The parental THP-1 cell line, derived from acute monocytic leukemia patient peripheral blood, is a well-established model for studying monocyte and macrophage biology. Following differentiation into macrophage-like cells, THP-1 cells recapitulate key inflammatory responses, including cytokine secretion and complement activation, making them a highly relevant host for examining C5 function in myeloid-driven immune processes.
C5 is a central component of the terminal complement cascade, cleaved by C5 convertase into C5a and C5b. C5a triggers potent pro-inflammatory signals through C5aR1 (CD88), promoting chemotaxis, NLRP3 inflammasome activation, reactive oxygen species production, and the release of IL-6, IL-8, and TNF-??. C5b initiates the sequential assembly of C6, C7, C8, and C9 into the membrane attack complex (MAC), causing cell lysis. C5 expression is regulated by upstream stimuli including LPS, TNF-??, IL-6, and IFN-?? via NF-??B and STAT3 pathways, and its cleavage is modulated by interacting factors such as C3b, complement factor B, complement factor D, and properdin.
Disruption of C5 in THP-1 cells abolishes both C5a signaling and MAC formation, creating a clean loss-of-function model for complement-dependent macrophage responses. This cell line is therefore invaluable for probing how complement dysregulation contributes to diseases like paroxysmal nocturnal hemoglobinuria, atypical hemolytic uremic syndrome, complement-mediated kidney diseases, and age-related macular degeneration, and for testing the specificity of C5-targeted therapeutics.
Research applications include mechanistic studies of complement-mediated inflammation, high-throughput screening of C5 inhibitors or anti-C5 antibodies, and modeling of terminal pathway deficiencies. Standard assays used with this knockout line include C5a ELISA, MAC deposition flow cytometry, C5a-induced chemotaxis assays, cytokine multiplex analysis, and western blotting for pathway validation. This cell line enables detailed functional dissection in a relevant macrophage system. For additional details, please contact Ascent Research.
