Lipid Carriers
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.
- Apolipoprotein Antibodies and Conjugates >
- Apolipoprotein Bioactive Proteins >
- Apolipoprotein ELISA Kits >
- Apolipoprotein Proteome Profiler® Antibody Arrays >
Fatty acid binding proteins (FABP) shuttle lipids, cholesterol, and other hydrophobic molecules between cellular membranes and through the cytoplasm.
Lipoprotein Particle Metabolism
Lipid Metabolism Enzymes
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.
- Lipid Core Modification: Endothelial lipase, CETP & PLTP Antibodies and Conjugates
- Lipid Core Modification Bioactive Proteins (at R&D Systems) >
- Lipid Core Modification Small Molecules (at R&D Systems) >
Adipokine Tools
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.
Oxidase Tools
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.
Lipoprotein Particle Uptake
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. Leptin has also been found to reduce LDLR levels in hepatocyte via the PCSK9 pathway.
- Lipoprotein Particle Receptor Antibodies and Conjugates >
- Lipoprotein Particle Receptor Bioactive Proteins >
- Lipoprotein Particle Receptor ELISA Kits >
- PCSK9 Simple Plex Assay >
- PCSK9 Inhibitor >
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. Additionally, proteins such as GAPDH are essential to general metabolism, particularly glycolysis. Since GAPDH is expressed at high levels in most tissues, it is useful as protein loading control in Western Blot analysis.
Intracellular Metabolism
Internalized fatty acids are broken down by mitochondrial beta-oxidation to acetyl-CoA which feeds into the tricarboxylic acid (TCA or Krebs) cycle. Adipocytes are specialized cells that balance lipid catabolism with storage of excess fatty acids in lipid droplets. Lipid droplets are dynamic structures that change in size, subcellular location and protein content. 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.
