Author Correction ERK5 is required for VEGF-mediated survival and tubular morphogenesis of primary human microvascular endothelial cells
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In Fig. 4, the concentration of staurosporine (STS) was mistakenly given as 50 mM, rather than the correct concentration of 50 nM (lines 9 and 15 in the legend). Moreover, the first sentence in the 'Signal transduction inhibitors' section in the Materials and Methods (page 3198) should read: Rapamycin, staurosporine and wortmannin were purchased from Calbiochem (Merck Chemicals Ltd, Nottingham, UK) and reconstituted in DMSO (Sigma). Introduction Angiogenesis defines the formation of new blood vessels from pre-existing vessels and is crucial for normal physiological vascular development, as well as for the pathological development of certain diseases, including diabetic retinopathy, atherosclerosis and cancer (Carmeliet, 2005). VEGF is a potent inducer of angiogenesis and is vital for vascular development, both during embryogenesis and in early neonatal life (Carmeliet et al. It activates a number of receptor tyrosine kinases that are present on endothelial cells. VEGF receptor-1 (VEGFR-1/Flt-1) and VEGFR-2 (Flk-1/KDR) are present on vascular endothelial cells, whereas expression of VEGFR-3 (Flk-4) is confined to lymphatic endothelial cells (Cross et al., 2003; Lohela et al., 2009; Olsson et al., 2006). Numerous studies have revealed that activation of VEGFR-2 by the VEGF-A ligand is responsible for mediating the majority of physiological effects of VEGF in endothelial cells, including proliferation, migration, survival and permeability (Holmes et al., 2007). Identification of intracellular signalling pathways involved in VEGF–VEGFR-2 signalling has been subject to intense research in an attempt to decipher the crucial components downstream of VEGFR-2 (Holmes et al., 2007). Mitogen-activated protein kinases (MAPKs) regulate the transduction of extracellular growth factor or stress-induced stimuli from the cell membrane to nuclear or cytoplasmic targets, and are crucial for the control of numerous cellular processes, including proliferation, migration and survival in response to these
منابع مشابه
ERK5 is required for VEGF-mediated survival and tubular morphogenesis of primary human microvascular endothelial cells.
Extracellular signal-regulated kinase 5 (ERK5) is activated in response to environmental stress and growth factors. Gene ablation of Erk5 in mice is embryonically lethal as a result of disruption of cardiovascular development and vascular integrity. We investigated vascular endothelial growth factor (VEGF)-mediated ERK5 activation in primary human dermal microvascular endothelial cells (HDMECs)...
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تاریخ انتشار 2010