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Growth factors (also known as trophic factors) bind to cell-surface receptors to initiate signaling pathways that result in the growth and differentiation of numerous different cell types. Their effect on cell growth is particularly relevant in cancer research.
Growth factors initiate numerous different signaling cascades in order to regulate cell differentiation and proliferation. The growth/survival signal is initially carried by these receptor ligands - proteins such as epidermal growth factor (EGF), fibroblast growth factor (FGF) and vascular endothelial growth factor (VEGF) - which bind cell-surface receptor tyrosine kinases (RTKs). Additionally, transforming growth factor β signals through receptor serine/threonine kinases (RSTKs) and activates downstream SMAD proteins to regulate the expression of specific genes.
Receptor-mediated endocytosis helps terminate the growth factor signal by internalizing the ligand-receptor complex. However, mutant RTKs may continue to send proliferative signals even in the absence of growth factor stimulation. Deregulation of growth factor receptor activity is found in nearly all epithelial tumors, and the expression of mutant forms of growth factor proteins may also lead to cancer.
Although growth factors act on different cell types, the signal pathways they initiate often overlap: for example, both EGF and FGF ensure cell survival by activating PI 3-K and MAPK cascades. These shared mechanisms have generated large amounts of interest in the field of cancer research.
Tocris offers the following scientific literature for Growth Factor Receptors to showcase our products. We invite you to request* your copy today!
*Please note that Tocris will only send literature to established scientific business / institute addresses.
Written by Kirsty E. Clarke, Victoria B. Christie, Andy Whiting and Stefan A. Przyborski, this review provides an overview of the use of small molecules in the control of stem cell growth and differentiation. Key signaling pathways are highlighted, and the regulation of ES cell self-renewal and somatic cell reprogramming is discussed. Compounds available from Tocris are listed.