In Stock Cell Lines
The ANGPTL4 Knockout HK-2 Cell Line is a CRISPR/Cas9-edited knockout model with targeted disruption of the ANGPTL4 gene in human HK-2 kidney proximal tubule epithelial cells. ANGPTL4 encodes angiopoietin-like 4, a secreted regulator of lipoprotein lipase (LPL) and integrin signaling, controlled by PPAR?? and metabolic factors. This cell line is ideal for investigating renal lipid metabolism, diabetic nephropathy, and metabolic stress responses. It removes endogenous LPL inhibition, enabling studies of fatty acid uptake, signaling via PI3K/Akt, and PPAR agonist screening using assays such as LPL activity, BODIPY uptake, and RNA-seq.
C3ar1 Knockout AML12 Cell Line
Cat. No. ARG43766
INA Knockout Hela Polyclonal Cells
Cat. No. ARG26265
IDH1 Knockout HEK293T Polyclonal Cells
Cat. No. ARG26103
APPL1 Knockout HAP1 Polyclonal Cells
Cat. No. ARG34705
FBXL18 Knockout 786-O Polyclonal Cells
Cat. No. ARG5034
Mouse Colonic Mucosal Epithelial Cells
Cat. No. ARP0470
The ANGPTL4 Knockout HK-2 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the human HK-2 proximal tubular epithelial cell line, featuring targeted disruption of the ANGPTL4 gene. This product provides a loss-of-function model for studying angiopoietin-like 4, a secreted inhibitor of lipoprotein lipase (LPL), without interference from endogenous ANGPTL4 expression. The cell line is suitable for diverse in vitro functional assays in renal biology and metabolic research.
HK-2 is an immortalized human kidney proximal tubule epithelial cell line derived from normal adult kidney. Proximal tubular cells carry out solute reabsorption and secretion, acid-base regulation, and renal metabolism. HK-2 is a widely used model for nephrotoxicity screening, renal disease investigation, and studies of tubular transport and metabolic function, providing a physiologically relevant host for exploring lipid handling and metabolic stress.
ANGPTL4 encodes a secreted glycoprotein that primarily inhibits LPL activity, thereby regulating plasma triglycerides and cellular fatty acid uptake. Its expression is upregulated by PPAR??, PPAR??, glucocorticoids, HIF-1??, TNF-??, and IL-1??, and by fasting/insulin signaling. ANGPTL4 interacts with LPL, integrins ??5??1, and heparan sulfate proteoglycans via its C-terminal fibrinogen-like domain. Downstream, it suppresses LPL-mediated hydrolysis, reduces free fatty acid uptake, and modulates integrin-dependent ITG??5??1-FAK signaling and the PI3K/Akt pathway. Representative components include VLDL, chylomicrons, CD36, FATP, and the PPAR??-RXR-PGC1?? complex.
In HK-2 cells, ANGPTL4 knockout removes the endogenous LPL inhibitor, potentially enhancing local lipid uptake and altering cellular energy metabolism and inflammatory signaling. This model enables dissection of ANGPTL4’s role in proximal tubular lipid handling and responses to injury, including processes relevant to diabetic nephropathy, obesity-related kidney injury, and acute kidney injury.
This cell line supports mechanistic studies of renal lipid metabolism, screening of PPAR agonists, and investigation of tubular responses to metabolic stress. Typical assays include western blotting, RT-qPCR, LPL activity measurements, BODIPY-labeled fatty acid uptake, cell migration, apoptosis (Annexin V), immunofluorescence for integrins, and RNA-seq. It is useful for evaluating ANGPTL4 as a therapeutic target. For further details or tailored applications, please contact Ascent Research.
