In Stock Cell Lines
Homo sapiens (Human)
Liver
Adherent
The ACSL5 Knockout HuH-7 Cell Line is a CRISPR/Cas9-edited knockout cell line engineered to disrupt ACSL5 in HuH-7 human hepatocellular carcinoma cells. ACSL5 encodes a long-chain fatty acyl-CoA synthetase critical for fatty acid activation, channeling lipids into ??-oxidation, triglyceride synthesis, and phospholipid production. It is regulated by PPAR?? and SREBP-1c and interacts with FATP2 and lipid droplet proteins. This knockout model impairs lipid metabolism, making it valuable for studying hepatic steatosis, hepatocellular carcinoma, and metabolic disorders. Suitable for assays including lipidomics, Oil Red O staining, and mitochondrial respiration measurements.
MTMR12 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16716
MSH3 Knockout K562 Polyclonal Cells
Cat. No. ARG19457
G3BP2 Knockout Hela Polyclonal Cells
Cat. No. ARG8497
HAVCR1 Knockout MCF7 Polyclonal Cells
Cat. No. ARG36435
DUSP10 Knockout Hela Polyclonal Cells
Cat. No. ARG40032
DYNLL2 Knockout Hela Polyclonal Cells
Cat. No. ARG40171
The ACSL5 Knockout HuH-7 Cell Line is a CRISPR/Cas9-edited knockout cell line that disrupts the ACSL5 gene in HuH-7 human hepatocellular carcinoma cells. This loss-of-function model enables stable and reproducible ablation of ACSL5 expression, facilitating detailed investigation of fatty acid metabolism and lipid signaling pathways in a hepatic context.
HuH-7 cells originate from a well-differentiated hepatocellular carcinoma of a 57-year-old male and retain liver-specific functions, making them an ideal model for liver cancer, hepatocyte metabolism, and viral hepatitis research. Their metabolic competence supports physiologically relevant studies of hepatic lipid handling, providing a robust background for interrogating ACSL5 function.
ACSL5 encodes a long-chain fatty acyl-CoA synthetase that catalyzes the thioesterification of fatty acids with coenzyme A, a critical activation step. It is transcriptionally regulated by PPAR??, SREBP-1c, ChREBP, and LXR, and responds to insulin, glucose, and polyunsaturated fatty acids. The resulting acyl-CoAs are directed to CPT1A for ??-oxidation, DGAT1/2 for triglyceride synthesis, and phospholipid biosynthetic enzymes, also contributing to pro-inflammatory eicosanoids. ACSL5 interacts with fatty acid transporters FATP2/4, lipid droplet proteins, and MBOAT7, and operates upstream of PPAR?? transcriptional programs controlling lipid catabolism and energy homeostasis.
In HuH-7 cells, ACSL5 disruption impairs fatty acid activation, reducing acyl-CoA pools. This compromises triglyceride and phospholipid synthesis, attenuates fatty acid oxidation, and dampens PPAR?? signaling. Consequently, the knockout model often exhibits reduced lipid accumulation, altered membrane composition, and modified cell proliferation??phenotypes relevant to hepatic steatosis, hepatocellular carcinoma, and metabolic syndrome. Thus, it serves as a powerful tool for dissecting lipid metabolic dysfunction.
This cell line supports diverse applications: mechanistic studies of lipid metabolism in liver cancer, lipid droplet dynamics, and drug screening for NAFLD. It is suitable for Western blotting, RT-qPCR, fatty acid oxidation assays, triglyceride quantification, Oil Red O staining, lipidomics, Seahorse respiration analysis, and flow cytometry. The model also enables transcriptomic and interactome studies to elucidate ACSL5-dependent networks. For further details, please contact Ascent Research.
