about
Frequently asked questions in hypoxia researchFIH Regulates Cellular Metabolism through Hydroxylation of the Deubiquitinase OTUB1REST is a hypoxia-responsive transcriptional repressorCrosstalk between Microbiota-Derived Short-Chain Fatty Acids and Intestinal Epithelial HIF Augments Tissue Barrier Function.Hypercapnia Suppresses the HIF-dependent Adaptive Response to Hypoxia.Hypoxia: from basic mechanisms to therapeutics - a meeting report on the Keystone and HypoxiaNet Symposium.Regulation of IL-1β-induced NF-κB by hydroxylases links key hypoxic and inflammatory signaling pathways.Hydroxylase-dependent regulation of the NF-κB pathway.MicroRNA-155 promotes resolution of hypoxia-inducible factor 1alpha activity during prolonged hypoxia.Paricalcitol protects against TGF-β1-induced fibrotic responses in hypoxia and stabilises HIF-α in renal epithelia.The functional interplay between the HIF pathway and the ubiquitin system - more than a one-way road.Intermittent hypoxia confers pro-metastatic gene expression selectively through NF-κB in inflammatory breast cancer cells.Carbon dioxide-dependent regulation of NF-κB family members RelB and p100 gives molecular insight into CO2-dependent immune regulation.REST mediates resolution of HIF-dependent gene expression in prolonged hypoxia.Editorial: a PHD in macrophage survival.Small ubiquitin-related modifier (SUMO)-1 promotes glycolysis in hypoxia.Loss of prolyl hydroxylase-1 protects against colitis through reduced epithelial cell apoptosis and increased barrier function.A dynamic model of the hypoxia-inducible factor 1α (HIF-1α) network.Genetic Knockdown and Pharmacologic Inhibition of Hypoxia-Inducible Factor (HIF) Hydroxylases.An intact canonical NF-κB pathway is required for inflammatory gene expression in response to hypoxia.A dynamic model of the hypoxia-inducible factor 1a (HIF-1a) networkGeneration of renal Epo-producing cell lines by conditional gene tagging reveals rapid HIF-2 driven Epo kinetics, cell autonomous feedback regulation, and a telocyte phenotypeHydroxylase Inhibition Selectively Induces Cell Death in MonocytesOxygen-dependent bond formation with FIH regulates the activity of the client protein OTUB1HIF hydroxylase inhibitors decrease cellular oxygen consumption depending on their selectivity
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description
researcher
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wetenschapper
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հետազոտող
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name
Carsten C Scholz
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Carsten C Scholz
@en
Carsten C Scholz
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Carsten C Scholz
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type
label
Carsten C Scholz
@ast
Carsten C Scholz
@en
Carsten C Scholz
@es
Carsten C Scholz
@nl
prefLabel
Carsten C Scholz
@ast
Carsten C Scholz
@en
Carsten C Scholz
@es
Carsten C Scholz
@nl
P106
P31
P496
0000-0001-6579-8015