In Stock Cell Lines
The Acer2 Knockout AML12 Cell Line is a CRISPR/Cas9-edited mouse hepatocyte line lacking alkaline ceramidase 2 activity, designed for studying sphingolipid metabolism in liver disease models. Disruption of Acer2 impairs ceramide hydrolysis, altering the balance between pro-apoptotic ceramides and pro-survival sphingosine-1-phosphate (S1P) signaling, with downstream impacts on Akt and ERK pathways. This model enables investigation of ceramide-driven apoptosis, steatosis, and insulin resistance in the context of NAFLD, liver fibrosis, and metabolic syndrome. It supports assays such as ceramide quantification, S1P ELISA, and viability tests, making it a valuable tool for drug screening and mechanistic research in hepatocyte biology.
FCHSD2 Knockout jurkat Polyclonal Cells
Cat. No. ARG13297
AGO3 Knockout Raji Polyclonal Cells
Cat. No. ARG21094
MBD6 Knockout CaSki Polyclonal Cells
Cat. No. ARG9787
LRRC57 Knockout MES-OV Polyclonal Cells
Cat. No. ARG5908
MAP2K2 Knockout 786-O Polyclonal Cells
Cat. No. ARG5314
NCI-H647
Cat. No. ARC0647
The Acer2 Knockout AML12 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from AML12 mouse hepatocytes, with targeted disruption of the Acer2 gene. This loss-of-function model provides a stable system to investigate the role of alkaline ceramidase 2 in hepatic sphingolipid metabolism. By eliminating Acer2 activity, it enables dissection of ceramide-dependent pathways affecting hepatocyte function without transient knockdown limitations.
AML12 cells are immortalized hepatocytes from the CD1 strain transgenic for human TGF-alpha, maintaining differentiated liver functions including protein synthesis, bile production, and metabolic detoxification. As a parenchymal cell line, AML12 offers a physiologically relevant platform for studying hepatocyte biology, making it ideal for gene-editing approaches to dissect liver-specific processes in lipid handling and stress responses.
Acer2 encodes an alkaline ceramidase that hydrolyzes ceramides to sphingosine and free fatty acid, a key step in sphingolipid catabolism. Its expression is modulated by upstream factors such as TNF-alpha, interferon-gamma, p53, and PPAR-alpha. Acer2-generated sphingosine serves as a substrate for sphingosine-1-phosphate (S1P) synthesis, which engages S1P receptors to activate downstream kinases Akt and ERK. The enzyme interacts with sphingosine kinase 2 and other ceramidases, positioning it at a critical node that controls the balance between pro-apoptotic ceramides and pro-survival S1P signals.
In AML12 hepatocytes, Acer2 knockout disrupts sphingolipid homeostasis, leading to ceramide accumulation and diminished sphingosine/S1P levels. This imbalance impairs cell survival and metabolic signaling, mirroring features of non-alcoholic fatty liver disease and liver fibrosis. The model is therefore valuable for examining how ceramide-mediated stress contributes to hepatocyte dysfunction, insulin resistance, and inflammatory cascades in chronic liver diseases.
This knockout cell line supports applications ranging from sphingolipid metabolism studies to drug screening for NAFLD/NASH. Representative assays include ceramide quantification by mass spectrometry, S1P ELISA, western blotting for cleaved caspase-3 and PARP, RT-qPCR for sphingolipid enzymes, and cell viability tests under lipotoxic challenge. It is also suitable for investigating ceramide-mediated apoptosis, steatosis, and S1P receptor signaling. For further information, contact Ascent Research.
