Pichia guilliermondii, Schwanniomyces occidentalis, Torulopsis candida and several riboflavin-dependent mutants of Torulopsis candida were grown in a medium with a low concentration of iron. In these conditions, the activity of GTP-cyclohydrolase which catalyzes the first step of flavinogenesis increases. The activity of the enzyme increases also when the cells of T. candida and P. guilliermondii with a high content of iron are incubated with alpha, alpha'-dipyridyl which induces overproduction of riboflavin; this action of alpha, alpha'-dipyridyl is eliminated by cycloheximide. Therefore, iron deficiency in the cells of these yeasts causes derepression of GTP-cyclohydrolase participating in riboflavin biosynthesis. The activity of the enzyme is inhibited by FAD but not by FMN and riboflavin.
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Front Pharmacol
March 2024
Shanghai Key Laboratory of Psychotic Disorders, Brain Health Institute, National Center for Mental Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
The α2-adrenoceptor agonist dexmedetomidine is a commonly used drug for sedatives in clinics and has analgesic effects; however, its mechanism of analgesia in the spine remains unclear. In this study, we systematically used behavioural and transcriptomic sequencing, pharmacological intervention, electrophysiological recording and ultrasound imaging to explore the analgesic effects of the α2-adrenoceptor and its molecular mechanism. Firstly, we found that spinal nerve injury changed the spinal transcriptome expression, and the differential genes were mainly related to calcium signalling and tissue metabolic pathways.
View Article and Find Full Text PDFEur J Pharmacol
March 2024
Department of Genetics and Endocrine, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, 510623, China. Electronic address:
Dopa and tetrahydrobiopterin (BH4) supplementation are recommended therapies for the dopa-responsive dystonia caused by GTP cyclohydrolase 1 (GCH1, also known as GTPCH) deficits. However, the efficacy and mechanisms of these therapies have not been intensively studied yet. In this study, we tested the efficacy of dopa and BH4 therapies by using a novel GTPCH deficiency mouse model, Gch1, which manifested infancy-onset motor deficits and growth retardation similar to the patients.
View Article and Find Full Text PDFJ Exp Clin Cancer Res
October 2022
Department of Neurosurgery, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, 200072, China.
Background: Ferroptosis is a novel form of iron-dependent cell death and participates in the malignant progression of glioblastoma (GBM). Although circular RNAs (circRNAs) are found to play key roles in ferroptosis via several mechanisms, including regulating iron metabolism, glutathione metabolism, lipid peroxidation and mitochondrial-related proteins, there are many novel circRNAs regulating ferroptosis need to be found, and they may become a new molecular treatment target in GBM.
Methods: The expression levels of circLRFN5, PRRX2 and GCH1 were detected by qPCR, western blotting, and immunohistochemistry.
Sci Rep
August 2022
Institute of Systems Motor Science, Center of Brain, Behavior and Metabolism, Universität zu Lübeck, Ratzeburger Allee 160, 23538, Lübeck, Germany.
Dopa-responsive dystonia (DRD) is caused by an impaired dopamine biosynthesis due to a GTP-cyclohydrolase-1 (GCH1) deficiency, resulting in a combination of dystonia and parkinsonism. However, the effect of GCH1 mutations and levodopa treatment on motor control beyond simple movements, such as timing, action preparation and feedback processing, have not been investigated so far. In an active time estimation task with trial-by-trial feedback, participants indicated a target interval (1200 ms) by a motor response.
View Article and Find Full Text PDFJ Vis Exp
May 2022
BHF Centre of Research Excellence, Division of Cardiovascular Medicine, Radcliffe Department of Medicine, John Radcliffe Hospital, University of Oxford; Wellcome Centre for Human Genetics, University of Oxford;
Macrophages are derived from hematopoietic progenitor cells throughout the body, are central to inflammatory processes, and participate in innate and adaptive immune responses. In vitro study of macrophages can be undertaken by ex vivo culture from the peritoneum or through differentiation of myeloid bone marrow progenitor cells to form bone marrow-derived macrophages (BMDMs). A common approach to macrophage differentiation from precursors involves the use of conditioned media from L929 cells (LCM).
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