Negative regulation of hypoxia-inducible genes by the von Hippel-Lindau protein
作者： O. Iliopoulos , A. P. Levy , C. Jiang , W. G. Kaelin , M. A. Goldberg
关键词: Cell biology 、 GLUT1 、 Endocrinology 、 Vascular endothelial growth factor 、 Biology 、 Glucose transporter 、 Vascular endothelial growth factor A 、 Glucose Transporter Type 1 、 Internal medicine 、 Growth factor 、 Platelet-derived growth factor 、 Von Hippel–Lindau tumor suppressor
摘要: Inactivation of the von Hippel-Lindau protein (pVHL) has been implicated in pathogenesis renal carcinomas and central nervous system hemangioblastomas. These are highly vascular tumors which overproduce angiogenic peptides such as endothelial growth factor/vascular permeability factor (VEGF/VPF). Renal carcinoma cells lacking wild-type pVHL were found to produce mRNAs encoding VEGF/VPF, glucose transporter GLUT1, platelet-derived B chain under both normoxic hypoxic conditions. Reintroduction wild-type, but not mutant, into these specifically inhibited production conditions, thus restoring their previously described hypoxia-inducible profile. Thus, appears play a critical role transduction signals generated by changes ambient oxygen tension.
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