In Stock Cell Lines
Homo sapiens (Human)
Heart
Adherent
The IL1RL1 Knockout AC16 Cell Line is a CRISPR/Cas9-edited human adult ventricular cardiomyocyte model with a disrupted IL1RL1 gene, eliminating ST2 receptor expression. It provides a robust platform for loss-of-function studies in a cardiac-relevant cellular context. IL1RL1 encodes ST2, the receptor for IL-33, which upon ligand binding activates NF-??B and MAPK/ERK cascades via IL-1RAcP/MyD88/IRAK/TRAF6 signaling, promoting pro-inflammatory cytokines (IL-6, IL-8) and fibrotic factors (collagen). This cell line is widely applied in cardiac hypertrophy research, myocardial fibrosis investigations, IL-33/ST2 pathway analysis, and drug screening for heart failure.
Immortalized Human Ovarian Epithelial Cell
Cat. No. ARI0330
GSTK1 Knockout K562 Polyclonal Cells
Cat. No. ARG20511
GLUD1 Knockout A2780 Polyclonal Cells
Cat. No. ARG18461
EGF Knockout Raji Polyclonal Cells
Cat. No. ARG40718
CHAC2 Knockout MES-OV Polyclonal Cells
Cat. No. ARG6254
NOTCH3 Knockout AGS Polyclonal Cells
Cat. No. ARG3143
The IL1RL1 Knockout AC16 Cell Line is a CRISPR/Cas9-edited human cardiomyocyte knockout model in which the IL1RL1 gene has been functionally disrupted. This cell line provides a defined genetic background for investigating the role of the IL1RL1-encoded ST2 receptor in cardiac inflammatory and fibrotic signaling. By eliminating endogenous ST2 expression, researchers can dissect IL-33-dependent responses and downstream effector pathways in a ventricular cardiomyocyte context.
The AC16 cell line is derived from human adult ventricular cardiomyocytes and retains essential features of contractile cardiac muscle cells, including the expression of cardiac-specific markers and the capacity for hypertrophic and stress responses. As an immortalized yet functionally relevant model, AC16 cells enable reproducible in vitro studies of cardiomyocyte biology, offering a consistent platform for examining gene function, signaling transduction, and pharmacological interventions in a human cardiac system.
IL1RL1 encodes ST2, the receptor for interleukin-33 (IL-33). Upon IL-33 binding, ST2 heterodimerizes with IL-1RAcP, recruiting MyD88 and activating IRAK1/4 and TRAF6. This activates NF-??B and MAPK/ERK pathways, driving transcription of pro-inflammatory cytokines (IL-6, IL-8), chemokine CCL2, and fibrotic factors like collagen. The pathway is modulated by upstream regulators TNF-??, IL-1??, and mechanical stress.
In AC16 cardiomyocytes, ST2 signaling is crucial in cardiac remodeling, including hypertrophy and fibrosis leading to heart failure. This knockout cell line enables the dissection of cardiomyocyte-intrinsic IL-33/ST2 effects, separating them from fibroblast and immune cell contributions. It provides a valuable model for studying maladaptive responses and testing therapeutic interventions.
This model supports IL-33 stimulation assays, phospho-ERK/NF-??B luciferase reporter assays, qPCR, Western blotting, and ELISA for IL-6/IL-8. Hypertrophy assays (cell size, ANP) and fibrosis marker expression (collagen, fibronectin) can be performed. The cell line is ideal for drug screening in heart failure, inflammatory response studies, and IL-33/ST2 pathway analysis. For further information, contact Ascent Research.
