Quiescent hypervascularity mediated by gain of HIF-1 alpha function.
Arbeit
J M
JM
UCSF Comprehensive Cancer Center, Department of Surgery, University of California, San Francisco, California 94143-0808, USA.
D043925:Angiogenesis Inducing Agents / Q000235:genetics / Q000502:physiology; D000818:Animals; D002199:Capillary Permeability; D015316:Genetic Therapy; D018380:Hematopoietic Stem Cell Transplantation; D006801:Humans; D000860:Hypoxia / Q000235:genetics / Q000503:physiopathology / Q000628:therapy; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D051379:Mice; D008833:Microcirculation / Q000254:growth & development / Q000502:physiology; D008955:Models, Cardiovascular; D018919:Neovascularization, Physiologic / Q000235:genetics*; D014157:Transcription Factors / Q000235:genetics* / Q000502:physiology*; D042461:Vascular Endothelial Growth Factor A
D043925:Angiogenesis Inducing Agents; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D014157:Transcription Factors; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse