Metabolic signalling pathways play crucial roles in regulating various metabolic processes within both normal and cancer cells. These signalling pathways profoundly alter metabolism and can in turn generate altered levels of metabolites that can themselves alter cell signalling pathways, allowing cancer cells to respond differently to normal cells to such signals. Perhaps the best-known example is the insulin/PI3K signalling pathway which activates a signalling cascade in response to insulin or insulin-like growth factors. This signalling pathway is frequently dysregulated in tumours. Activation of phosphoinositide 3-kinase (PI3K) leads to activation of protein kinase B (AKT), which, in turn, activates mammalian target of rapamycin (mTOR). Activation of insulin/PI3K signalling leads to a variety of metabolic alterations, including the translocation of glucose transporters (GLUT4) to the cell membrane. In cancer cells this allows increased glucose uptake, promoting the altered metabolism characteristic of the Warburg effect and facilitating increased proliferation and survival. The AMP-activated Protein Kinase (AMPK) pathway is another important player in metabolic signalling. AMPK is an energy-sensing protein kinase that monitors cellular energy status via detection of a high AMP/ATP ratio. When cellular energy levels are low (e.g., during nutrient deprivation), AMPK is activated. Upon activation, AMPK phosphorylates various downstream targets, leading to increased glucose uptake, fatty acid oxidation, and inhibition of energy-consuming processes like fatty acid, cholesterol and protein synthesis. Another important regulator of protein synthesis is the mTOR (mechanistic Target of Rapamycin) pathway. mTOR is a key regulator of multiple processes regulating cell growth, metabolism, and autophagy, integrating signals from nutrients, growth factors, and energy availability. Activation of mTOR promotes biosynthetic processes, including protein and lipid biosynthesis, whilst inhibiting catabolic processes like autophagy. Lipid biosynthesis is proximally regulated by the Peroxisome Proliferator-Activated Receptors (PPARs) pathway: PPARs are nuclear receptor transcription factors that regulate the expression of genes involved in lipid uptake, storage, and oxidation. They are activated in cells by fatty acids and their derivatives. Once activated, PPARs form heterodimers with retinoid X receptors (RXRs) and bind to specific DNA sequences. The Sterol Regulatory Element-Binding Proteins (SREBPs) are also transcription factors that also regulate lipid metabolism, including the synthesis of cholesterol and fatty acids. When cellular cholesterol levels are low, SREBP activation occurs. This pathway involves the proteolytic processing of SREBPs and subsequent translocation to the nucleus, where it binds to specific target genes involved in lipid synthesis. Finally, sirtuins are a family of NAD+-dependent deacetylases that regulate cellular metabolism and stress response. Sirtuins can modulate multiple metabolic pathways, such as glycolysis, oxidative phosphorylation, and fatty acid metabolism, and their dysregulation is implicated in cancer development and progression. We provide a wide product catalogue of research tools for investigating metabolic signaling pathways, including GAPDH antibodies, CD147 antibodies, Tyrosine Hydroxylase antibodies, Apolipoprotein E ELISA Kits, and POMC ELISA Kits. Explore our full metabolic signaling pathways product range below and discover more, for less. Alternatively, you can explore our Metabolism of Lipids & Lipoproteins, Metabolism of Carbohydrates, and Integration of Energy Metabolism product ranges.