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Jeroen Buters

Researcher at Technische Universität München

Publications -  153
Citations -  7708

Jeroen Buters is an academic researcher from Technische Universität München. The author has contributed to research in topics: Pollen & Aerobiology. The author has an hindex of 45, co-authored 137 publications receiving 6722 citations. Previous affiliations of Jeroen Buters include National Institutes of Health & University of Bern.

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Paclitaxel-resistant Human Ovarian Cancer Cells Have Mutant β-Tubulins That Exhibit Impaired Paclitaxel-driven Polymerization

TL;DR: Results identify residues β270 and β364 as important modulators of paclitaxel’s interaction with tubulin as well as acquired mutations in the M40 isotype at nucleotide 810 (T → G; Phe270 → Val) in 1A9PTX10 cells and nucleotide 1092 (G → A; Ala364 → Thr) in1A 9PTX22 cells.
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Role of CYP2E1 in the Hepatotoxicity of Acetaminophen

TL;DR: When cyp2e1 knockout mice were challenged with the common analgesic acetaminophen, they were found to be considerably less sensitive to its hepatotoxic effects than wild-type animals, indicating that this P-450 is the principal enzyme responsible for the metabolic conversion of the drug to its active hepatot toxic metabolite.
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Cytochrome P450 CYP1B1 determines susceptibility to 7,12-dimethylbenz[a]anthracene-induced lymphomas

TL;DR: CYP1B1-null mice, created by targeted gene disruption in embryonic stem cells, were born at the expected frequency from heterozygous matings with no observable phenotype as discussed by the authors.
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Meteorological conditions, climate change, new emerging factors, and asthma and related allergic disorders. A statement of the World Allergy Organization

TL;DR: Global warming is expected to affect the start, duration, and intensity of the pollen season, and the rate of asthma exacerbations due to air pollution, respiratory infections, and/or cold air inhalation, and other conditions on the other hand.
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Protection against Acetaminophen Toxicity in CYP1A2 and CYP2E1 Double-Null Mice ☆

TL;DR: The protection against APAP toxicity afforded by deletion of both CYP2E1 and CYP1A2 likely reflects greatly diminished production of the toxic electrophile, NAPQI.