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Michael S. Wiesener

Researcher at University of Erlangen-Nuremberg

Publications -  92
Citations -  12224

Michael S. Wiesener is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Hypoxia-inducible factors & Hypoxia (medical). The author has an hindex of 41, co-authored 79 publications receiving 11116 citations. Previous affiliations of Michael S. Wiesener include Humboldt University of Berlin & Wellcome Trust Centre for Human Genetics.

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The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis

TL;DR: It is indicated that the interaction between HIF-1 and pVHL is iron dependent, and that it is necessary for the oxygen-dependent degradation of HIF α-subunits, which may underlie the angiogenic phenotype of VHL-associated tumours.
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Widespread hypoxia-inducible expression of HIF-2alpha in distinct cell populations of different organs.

TL;DR: Data indicate that Hif‐2 plays an important role in the transcriptional response to hypoxia in vivo, which is not confined to the vasculature and is complementary to rather than redundant with HIF‐1.
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Expression of hypoxia-inducible factor-1alpha and -2alpha in hypoxic and ischemic rat kidneys.

TL;DR: In this paper, high-amplification immunohistochemical analyses were used to study the expression of HIF-1alpha and -2alpha in kidneys of rats exposed to systemic hypoxia bleeding anemia, functional anemia (01% carbon monoxide), renal ischemia, or cobaltous chloride (which is known to mimic hyperoxia) and showed that these treatments led to marked nuclear accumulation of these transcription factors in different renal cell populations.
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Differentiating the functional role of hypoxia-inducible factor (HIF)-1α and HIF-2α (EPAS-1) by the use of RNA interference: erythropoietin is a HIF-2α target gene in Hep3B and Kelly cells

TL;DR: A remarkably restricted target gene specificity of the HIFα subunits is found, which can be overcome in cells with perturbations in the pVHL/HIF system and under forced expression.