In Stock Cell Lines
The C3ar1 Knockout AML12 Cell Line is a CRISPR/Cas9-edited mouse hepatocyte cell line with targeted disruption of the C3ar1 gene, which encodes the complement C3a receptor. Derived from the non-tumorigenic AML12 line, these cells retain differentiated liver functions and provide a physiologically relevant model for studying C3aR signaling in hepatic inflammation. C3aR is a GPCR that, upon binding C3a, activates G??i/G??q-mediated pathways leading to ERK1/2 phosphorylation and NF-??B-driven cytokine production (IL-6, CXCL1). This knockout cell line is ideal for investigating complement-mediated liver injury, evaluating C3aR antagonists, and modeling diseases such as nonalcoholic steatohepatitis.
DGCR6L Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG18034
AMPD2 Knockout MES-OV Polyclonal Cells
Cat. No. ARG24127
INPPL1 Knockout A2780 Polyclonal Cells
Cat. No. ARG29227
HNRNPA3 Knockout Hela Polyclonal Cells
Cat. No. ARG37549
AVL9 Knockout HAP1 Polyclonal Cells
Cat. No. ARG27364
PHF10 Knockout HEK293T Polyclonal Cells
Cat. No. ARG4229
The C3ar1 Knockout AML12 Cell Line is a CRISPR/Cas9-mediated knockout cell line derived from the AML12 mouse hepatocyte cell line. It features targeted disruption of the C3ar1 gene, which encodes the complement C3a receptor 1 (C3aR), a G protein-coupled receptor that binds the anaphylatoxin C3a. This loss-of-function model abolishes C3aR expression, enabling precise dissection of C3a-mediated signaling in hepatocytes.
The AML12 host cell line is a non-tumorigenic hepatocyte line established from a transgenic mouse expressing human TGF-??. These cells maintain key differentiated functions, including albumin secretion and cytochrome P450 activity, providing a robust and physiologically relevant hepatic model. Their stable phenotype makes them well-suited for genetic manipulation and longitudinal studies of liver cell biology.
Upon binding of its ligand C3a, C3aR couples to G??i and G??q proteins, activating phospholipase C beta (PLCB) and generating second messengers IP3 and DAG. This triggers intracellular calcium mobilization and protein kinase C (PKC) activation, leading to ERK1/2 phosphorylation and NF-??B transcriptional activity. Downstream, NF-??B promotes expression of pro-inflammatory cytokines such as IL-6 and the chemokine CXCL1, as well as reactive oxygen species production. The signaling cascade is modulated by upstream regulators including TNF, IL-1??, and LPS, and involves receptor interaction with ??-arrestin for desensitization. Representative pathway components include C3, C3a, GNAI, GNAQ, PLCB, IP3, DAG, PKC, MAPK1, and NFKB1.
In hepatocytes, C3aR signaling contributes to inflammatory responses that drive liver pathologies such as acute injury, fibrosis, and nonalcoholic steatohepatitis (NASH). The C3ar1 Knockout AML12 Cell Line enables researchers to isolate hepatocyte-intrinsic C3aR functions from systemic complement effects, facilitating investigation of crosstalk between the complement system and hepatic metabolic pathways during stress and disease.
Key applications include C3a stimulation assays coupled with phospho-ERK western blot detection, cytokine secretion measurement (IL-6, CXCL1) by ELISA, and intracellular calcium flux analysis. The model supports RNA-sequencing to compare transcriptomes of wild-type and C3ar1-null hepatocytes, and can be used to test C3aR antagonists in disease-relevant contexts such as NASH and sepsis. For further technical details, please contact Ascent Research.
