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Fatty acids and cholesterol require carrier proteins to shield their hydrophobic regions as they move through body fluids. From fatty acid binding proteins to fatty acid transport proteins to apolipoproteins, we have the reagents and assays to advance your research.
Apolipoproteins function as structural components of lipoprotein particles and serve as binding proteins for cellular uptake of VLDL, LDL, and HDL.
Fatty acid binding proteins (FABP) shuttle lipids, cholesterol, and other hydrophobic molecules between cellular membranes and through the cytoplasm.
The lipid contents of circulating VLDL, LDL, and HDL can be shuttled between lipoprotein particles and released as free fatty acids by lipases. Oxidases act on lipids and apolipoproteins to generate pathogenic byproducts.
Free fatty acids are cleaved from triglycerides by Endothelial and Lipoprotein Lipases (EL and LPL). Phospholipids, triglycerides, and cholesteryl esters are transferred from the core of one particle to another by PLTP and CETP.
The regulation of lipid metabolism by EL and LPL is itself regulated by several adipokines including Adiponectin/Acrp30, Angiopoietin-like protein 3/ANGPTL3, and Angiopoietin-like 4/ANGPTL4.
Oxidized LDL formation is induced by Lipoxygenases, Myeloperoxidase, NOX, and PLA2G activity on both protein and lipid components. OxLDL formation is accelerated in conditions of oxidative stress and results in the generation of multiple proinflammatory molecules.
LDLR, VLDLR, LOX-1, and ApoER2 bind and internalize distinct classes of lipoprotein particles. PCSK9 inhibits the binding of LDL to LDLR and promotes intracellular LDLR degradation.
LDLR-related proteins (LRPs) are structurally related to LDLR and function as coreceptors for a variety of ligands including apolipoproteins.
Fatty acid transfer proteins (FATP) are multipass receptors that mediate fatty acid uptake across the plasma membrane and also promote fatty acid acylation.
Additional transporters mediate the cellular uptake of lipoprotein particles, including ABCA1, ABCG1, and the scavenger receptors CD36/SR-B3, SR-AI/MSR, and SR-BI.
Internalized fatty acids are broken down by mitochondrial beta-oxidation to acetyl-CoA which feeds into the Krebs cycle. Adipocytes are specialized cells that balance lipid catabolism with storage of excess fatty acids in lipid droplets. Fatty acid-sensitive transcription factors regulate the expression of enzymes involved in intracellular lipid metabolism.
We offer an extensive collection of reagents for lipid and cholesterol metabolism enzymes including inhibitors.Investigate Lipid Enzymes