|Human, Monkey, Mouse, Rat|
Application Methods: Immunoprecipitation, Western Blotting
Background: Apolipoproteins are plasma lipoproteins that function as transporters of lipids and cholesterol in the circulatory system. Chylomicrons are a fundamental class of apolipoproteins containing very low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL) (1,2).
Application Methods: Western Blotting
Background: Phospholipase A2 (PLA2) is a superfamily of enzymes that hydrolyze glycero-3-phosphocholines and release fatty acids and lysophospholipids (1). PLA2G1B is a member of this superfamily in the 1B group that is expressed most highly in the pancreatic acinar cells (2). Evidence suggests that PLA2G1B plays a role in the absorption and storage of extra energy as fats are metabolized (1,2). Lysophospholipids generated by PLA2G1B inhibit fatty acid oxidation in the liver and reduce energy expenditure, leading to diet-induced obesity and type 2 diabetes with a high fat diet (1). Therefore, a potential intervention of obesity and diabetes could target PLA2G1B in the digestive tract (2).
Application Methods: Flow Cytometry, Immunofluorescence (Immunocytochemistry), Immunoprecipitation, Western Blotting
Background: TNF-α, the prototypical member of the TNF protein superfamily, is a homotrimeric type-II membrane protein (1,2). Membrane-bound TNF-α is cleaved by the metalloprotease TACE/ADAM17 to generate a soluble homotrimer (2). Both membrane and soluble forms of TNF-α are biologically active. TNF-α is produced by a variety of immune cells including T cells, B cells, NK cells, and macrophages (1). Cellular response to TNF-α is mediated through interaction with receptors TNF-R1 and TNF-R2 and results in activation of pathways that favor both cell survival and apoptosis depending on the cell type and biological context. Activation of kinase pathways (including JNK, Erk1/2, p38 MAPK, and NF-κB) promotes the survival of cells, while TNF-α-mediated activation of caspase-8 leads to programmed cell death (1,2). TNF-α plays a key regulatory role in inflammation and host defense against bacterial infection, notably Mycobacterium tuberculosis (3).