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Erik Laughner

Researcher at Johns Hopkins University School of Medicine

Publications -  13
Citations -  9163

Erik Laughner is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Vascular endothelial growth factor A & Vascular endothelial growth factor. The author has an hindex of 12, co-authored 13 publications receiving 8796 citations. Previous affiliations of Erik Laughner include Johns Hopkins University.

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Cellular and developmental control of O2 homeostasis by hypoxia-inducible factor 1α

TL;DR: It is demonstrated that HIF-1alpha is a master regulator of cellular and developmental O2 homeostasis in Hif1a-/- embryos that manifested neural tube defects, cardiovascular malformations, and marked cell death within the cephalic mesenchyme.
Journal Article

Overexpression of Hypoxia-inducible Factor 1α in Common Human Cancers and Their Metastases

TL;DR: The first clinical data indicating that HIF-1alpha may play an important role in human cancer progression are provided, indicating adaptations to a hypoxic microenvironment that are correlated with tumor invasion, metastasis, and lethality.
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Modulation of Hypoxia-inducible Factor 1α Expression by the Epidermal Growth Factor/Phosphatidylinositol 3-Kinase/PTEN/AKT/FRAP Pathway in Human Prostate Cancer Cells: Implications for Tumor Angiogenesis and Therapeutics

TL;DR: It is demonstrated that in human prostate cancer cells, basal-, growth factor- and mitogen-induced expression of hypoxia-inducible factor 1 (HIF-1) alpha, the regulated subunit of the transcription factor Hif-1, is blocked by LY294002 and rapamycin, inhibitors of PI3K and FRAP, respectively.
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HER2 (neu) Signaling Increases the Rate of Hypoxia-Inducible Factor 1α (HIF-1α) Synthesis: Novel Mechanism for HIF-1-Mediated Vascular Endothelial Growth Factor Expression

TL;DR: It is demonstrated that HER2 signaling induced by overexpression in mouse 3T3 cells or heregulin stimulation of human MCF-7 breast cancer cells results in increased HIF-1α protein and VEGF mRNA expression that is dependent upon activity of PI3K, AKT, and the downstream kinase FRAP.
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Defective Vascularization of HIF-1α-Null Embryos Is Not Associated with VEGF Deficiency but with Mesenchymal Cell Death

TL;DR: In tissue culture cells, VEGF mRNA expression was induced by glucose deprivation independent of HIF-1alpha, providing a mechanism for increased VEGf mRNA expression in Hif1a-/- embryos, in which absence of adequate tissue perfusion resulted in both O2 and glucose deprivation.