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Gregg L. Semenza

Researcher at Johns Hopkins University School of Medicine

Publications -  524
Citations -  143292

Gregg L. Semenza is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Hypoxia (medical) & Transcription factor. The author has an hindex of 168, co-authored 502 publications receiving 130316 citations. Previous affiliations of Gregg L. Semenza include Max Delbrück Center for Molecular Medicine & University of Maryland, Baltimore.

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Targeting HIF-1 for cancer therapy

Gregg L. Semenza
- 01 Oct 2003 - 
TL;DR: Hypoxia-inducible factor 1 (HIF-1) activates the transcription of genes that are involved in crucial aspects of cancer biology, including angiogenesis, cell survival, glucose metabolism and invasion.
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Hypoxia-inducible factor 1 is a basic-helix-loop-helix-PAS heterodimer regulated by cellular O2 tension

Guang L. Wang, +3 more
- 06 Jun 1995 - 
TL;DR: Hypoxia-inducible factor 1 (HIF-1) is found in mammalian cells cultured under reduced O2 tension and is necessary for transcriptional activation mediated by the erythropoietin gene enhancer in hypoxic cells.
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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Activation of vascular endothelial growth factor gene transcription by hypoxia-inducible factor 1.

Jo A. Forsythe, +6 more
- 01 Sep 1996 - 
TL;DR: HIF-1 is implicate in the activation of VEGF transcription in hypoxic cells and this work demonstrates the involvement of Hif-1 in theactivation of V EGF transcription.
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HIF-1-mediated expression of pyruvate dehydrogenase kinase: A metabolic switch required for cellular adaptation to hypoxia

Jung Whan Kim, +3 more
- 01 Mar 2006 - 
TL;DR: A hypoxia-induced metabolic switch that shunts glucose metabolites from the mitochondria to glycolysis to maintain ATP production and to prevent toxic ROS production is revealed.