104 papers found
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NADPH oxidases, isoprostanes and NO in hypoxic pulmonary remodeling: Role of HIF transcription factors : Säule B: DZHK B 13-052 A : Abschlussbericht : Laufzeit des Projektes: 15.07.2013-30.09.2015
Folic Acid Promotes Recycling of Tetrahydrobiopterin and Protects Against Hypoxia-Induced Pulmonary Hypertension by Recoupling Endothelial Nitric Oxide Synthase
Deficiency of HIF1α in Antigen-Presenting Cells Aggravates Atherosclerosis and Type 1 T-Helper Cell Responses in Mice
Mitochondrial Dysfunction Due to Lack of Manganese Superoxide Dismutase Promotes Hepatocarcinogenesis
Calcium and ROS: A mutual interplay
Reactive oxygen species, nutrition, hypoxia and diseases: Problems solved?
Superoxide-Generating Nox5α Is Functionally Required for the Human T-Cell Leukemia Virus Type 1-Induced Cell Transformation Phenotype
Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair
NOX1 Supports the Metabolic Remodeling of HepG2 Cells
Einfluss von Redoxstress auf das Ubiquitin-Proteasom-System : Säule B: DZHK B 13-048 A : Abschlussbericht : Laufzeit des Projektes: 15.07.2013-30.09.2015
Targeting Tumour Hypoxia to Prevent Cancer Metastasis. From Biology, Biosensing and Technology to Drug Development: the METOXIA Consortium
Comparative characterization of cellular and molecular anti-restenotic profiles of paclitaxel and sirolimus. Implications for local drug delivery.
The beta 3-Integrin Binding Protein beta 3-Endonexin Is a Novel Negative Regulator of Hypoxia-Inducible Factor-1
Hypoxia and Reactive Oxygen Species
The role of nitric oxide radicals in removal of hyper-radiosensitivity by priming irradiation
Accounting for biological variation in differential display two-dimensional electrophoresis experiments
NADPH oxidases and the HIF pathway: An emerging liaison in vascular cells
The HIF1 target gene NOX2 promotes angiogenesis through urotensin-II
GSK-3 regulates cell growth, migration, and angiogenesis via Fbw7 and USP28-dependent degradation of HIF-1
Inhibition of endothelial nitric oxyde synthase increases capillary formation via Rac1-dependent induction of hypoxia-inducible factor-1α and plasminogen activator inhibitor-1: Thromb
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